Evidence map›Paper›PMID 22745494›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Oxidative phosphorylation, not glycolysis, powers presynaptic and postsynaptic mechanisms underlying brain information processing.

Catherine N Hall, Miriam C Klein-Flügge, Clare Howarth, David Attwell

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 281 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
281citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

281 citing papers in PubMed, 2 syntheses or guidelines pooled it, 459 citations in OpenAlex.

  1. Pooled it
  2. Systematic review ofFrontiers in aging neuroscience · 2023
    Pooled it
  3. Mitochondrial molecular diversity in the brain.Current opinion in neurobiology · 2026
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    Review
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  17. Targeting ATScientific reports · 2026
    Article
  18. Article
  19. Brain-derived ketone bodies can replace glucose to power neural function.bioRxiv : the preprint server for biology · 2026
    Article
  20. Article

221 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Catherine N HallDepartment of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, United Kingdom.
Miriam C Klein-Flügge
Clare Howarth
David Attwell
University College London · GB

Funding

Wellcome Trust 017948Wellcome Trust 075232
6 · The paper itself

Abstract

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.

Indexed as

Oxidative Phosphorylation6-Cyano-7-nitroquinoxaline-2,3-dioneAction PotentialsAdenosine TriphosphateAnimalsAnimals, NewbornCadmium ChlorideDose-Response Relationship, DrugElectric StimulationEnzyme InhibitorsExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsGlycolysisHippocampusIn Vitro TechniquesLactic Acid2-amino-5-phosphopentanoic acid6-Cyano-7-nitroquinoxaline-2,3-dioneAdenosine TriphosphateCadmium ChlorideEnzyme InhibitorsExcitatory Amino Acid AntagonistsLactic AcidNADOrganic Chemicalsoxamate (repellent)OxygenSodium Channel BlockersTetrodotoxinValine

Identifiers

PMID22745494
PMCPMC3390246
OpenAlexW2069821327

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.