|Oxidative phosphorylation, not glycolysis, powers presynaptic and postsynaptic mechanisms underlying brain information processing.|
|PMID: 22745494 Owner: NLM Status: MEDLINE|
|Neural activity has been suggested to initially trigger ATP production by glycolysis, rather than oxidative phosphorylation, for three reasons: glycolytic enzymes are associated with ion pumps; neurons may increase their energy supply by activating glycolysis in astrocytes to generate lactate; and activity increases glucose uptake more than O₂ uptake. In rat hippocampal slices, neuronal activity rapidly decreased the levels of extracellular O₂ and intracellular NADH (reduced nicotinamide adenine dinucleotide), even with lactate dehydrogenase blocked to prevent lactate generation, or with only 20% superfused O₂ to mimic physiological O₂ levels. Pharmacological analysis revealed an energy budget in which 11% of O₂ use was on presynaptic action potentials, 17% was on presynaptic Ca²⁺ entry and transmitter release, 46% was on postsynaptic glutamate receptors, and 26% was on postsynaptic action potentials, in approximate accord with theoretical brain energy budgets. Thus, the major mechanisms mediating brain information processing are all initially powered by oxidative phosphorylation, and an astrocyte-neuron lactate shuttle is not needed for this to occur.|
|Catherine N Hall; Miriam C Klein-Flügge; Clare Howarth; David Attwell|
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|Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't|
|Title: The Journal of neuroscience : the official journal of the Society for Neuroscience Volume: 32 ISSN: 1529-2401 ISO Abbreviation: J. Neurosci. Publication Date: 2012 Jun|
|Created Date: 2012-06-29 Completed Date: 2012-09-10 Revised Date: 2013-07-12|
Medline Journal Info:
|Nlm Unique ID: 8102140 Medline TA: J Neurosci Country: United States|
|Languages: eng Pagination: 8940-51 Citation Subset: IM|
|Department of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, United Kingdom.|
|APA/MLA Format Download EndNote Download BibTex|
Action Potentials / drug effects, physiology
Adenosine Triphosphate / metabolism
Cadmium Chloride / pharmacology
Dose-Response Relationship, Drug
Excitatory Amino Acid Antagonists / pharmacology
Excitatory Postsynaptic Potentials / drug effects
Glycolysis / physiology
Hippocampus / cytology*, physiology*
Lactic Acid / metabolism
NAD / metabolism
Neurons / cytology, drug effects, physiology*
Organic Chemicals / pharmacology
Oxidative Phosphorylation* / drug effects
Oxygen / metabolism, pharmacology
Presynaptic Terminals / drug effects, physiology*
Sodium Channel Blockers / pharmacology
Synapses / drug effects, physiology*
Tetrodotoxin / pharmacology
Valine / analogs & derivatives, pharmacology
|017948//Wellcome Trust; 075232//Wellcome Trust; //Wellcome Trust|
|0/Enzyme Inhibitors; 0/Excitatory Amino Acid Antagonists; 0/Organic Chemicals; 0/Sodium Channel Blockers; 10108-64-2/Cadmium Chloride; 115066-14-3/6-Cyano-7-nitroquinoxaline-2,3-dione; 4368-28-9/Tetrodotoxin; 50-21-5/Lactic Acid; 53-84-9/NAD; 56-65-5/Adenosine Triphosphate; 66257-53-2/oxamate (repellent); 7004-03-7/Valine; 76326-31-3/2-amino-5-phosphopentanoic acid; 7782-44-7/Oxygen|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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