| Oxidative phosphorylation, not glycolysis, powers presynaptic and postsynaptic mechanisms underlying brain information processing. | |
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MedLine Citation:
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PMID: 22745494 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Catherine N Hall; Miriam C Klein-Flügge; Clare Howarth; David Attwell |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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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 |
Date Detail:
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Created Date: 2012-06-29 Completed Date: 2012-09-10 Revised Date: 2013-03-14 |
Medline Journal Info:
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Nlm Unique ID: 8102140 Medline TA: J Neurosci Country: United States |
Other Details:
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Languages: eng Pagination: 8940-51 Citation Subset: IM |
Affiliation:
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Department of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, United Kingdom. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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6-Cyano-7-nitroquinoxaline-2,3-dione
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pharmacology Action Potentials / drug effects, physiology Adenosine Triphosphate / metabolism Animals Animals, Newborn Cadmium Chloride / pharmacology Dose-Response Relationship, Drug Electric Stimulation Enzyme Inhibitors Excitatory Amino Acid Antagonists / pharmacology Excitatory Postsynaptic Potentials / drug effects Glycolysis / physiology Hippocampus / cytology*, physiology* Lactic Acid / metabolism Models, Biological NAD / metabolism Neurons / cytology, drug effects, physiology* Organic Chemicals / pharmacology Oxidative Phosphorylation* / drug effects Oxygen / metabolism, pharmacology Presynaptic Terminals / drug effects, physiology* Rats Rats, Sprague-Dawley Sodium Channel Blockers / pharmacology Statistics, Nonparametric Synapses / drug effects, physiology* Tetrodotoxin / pharmacology Valine / analogs & derivatives, pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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017948//Wellcome Trust; 075232//Wellcome Trust; //Wellcome Trust |
| Chemical | |
Reg. No./Substance:
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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 |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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