Document Detail


Oxidative phosphorylation, not glycolysis, powers presynaptic and postsynaptic mechanisms underlying brain information processing.
MedLine Citation:
PMID:  22745494     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Catherine N Hall; Miriam C Klein-Flügge; Clare Howarth; David Attwell
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
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:
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    
Other Details:
Languages:  eng     Pagination:  8940-51     Citation Subset:  IM    
Affiliation:
Department of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, United Kingdom.
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MeSH Terms
Descriptor/Qualifier:
6-Cyano-7-nitroquinoxaline-2,3-dione / 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:
017948//Wellcome Trust; 075232//Wellcome Trust; //Wellcome Trust
Chemical
Reg. No./Substance:
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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