Glycolysis and recovery of potassium ion homeostasis and synaptic transmission in hippocampal slices after anoxia or stimulated potassium release.
The present study was undertaken to determine whether glycolytic energy production was critical to the survival of brain tissue subjected to metabolic stress. Specifically, the contributions of glycolysis (1) to recovery of ion homeostasis after anoxia or high frequency electrical stimulation, and (2) to recovery of synaptic transmission after anoxia, were examined. Energy metabolism in rat hippocampal slices was manipulated by varying glucose concentrations, and by substituting lactate for glucose. Ion transport was slower and recovery of synaptic transmission after anoxia was greatly impeded in the absence of glycolysis. These results support the hypothesis that glycolytic ATP production is tied directly or indirectly to ion transport. The results also suggest that recovery of synaptic transmission following anoxia requires glycolytic ATP.
Department of Neurology, University of Miami School of Medicine, FL.
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D000704:Analysis of Variance; D000818:Animals; D015687:Cell Hypoxia; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology; D006019:Glycolysis / Q000187:drug effects; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D006706:Homeostasis / Q000187:drug effects; D066298:In Vitro Techniques; D007461:Iodoacetates / Q000494:pharmacology; D019807:Iodoacetic Acid; D007700:Kinetics; D007773:Lactates / Q000378:metabolism; D011188:Potassium / Q000378:metabolism* / Q000494:pharmacology*; D051381:Rats; D011916:Rats, Inbred F344; D017208:Rats, Wistar; D013569:Synapses / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
D007461:Iodoacetates; D007773:Lactates; D005947:Glucose; D011188:Potassium; D019807:Iodoacetic Acid