ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
An increase in lactate output by brain tissue serves to meet the energy needs of glutamate-activated neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 291 citations in OpenAlex.
- Cerebral metabolic effects of exogenous lactate supplementation on the injured human brain.Intensive care medicine · 2014Trial
- Unveiling the "Glycolysis-Lactate-Lactylation" Axis: A Novel Target in Ischemic Cerebrovascular Disease.Neuroscience bulletin · 2026Review
- Article
- Histone lactylation modification and its role in cerebral ischemia-reperfusion injury (Review).Biomedical reports · 2026Review
- The glioma neuron symbiosis hypothesis-cellular and molecular mechanistic considerations.Frontiers in neuroscience · 2026Article
- Where Is the Oxygen? The Mirage of Non-Oxidative Glucose Consumption During Brain Activity.NeuroSci · 2025Review
- The Feud over Lactate and Its Role in Brain Energy Metabolism: An Unnecessary Burden on Research and the Scientists Who Practice It.International journal of molecular sciences · 2025Review
- Update on Neuroprotection after Traumatic Brain Injury.CNS drugs · 2025Review
- (Re)building the nervous system: A review of neuron-glia interactions from development to disease.Journal of neurochemistry · 2025Review
- Misprogramming of glucose metabolism impairs recovery of hippocampal slices from neuronal GLT-1 knockout mice and contributes to excitotoxic injury through mitochondrial superoxide production.Journal of neurochemistry · 2025Article
- Glioma neuron symbiosis: a hypothesis.Frontiers in neuroscience · 2025Article
- Dual role of lactate in human health and disease.Frontiers in physiology · 2025Review
- Lactate flux dysfunction in patients with bipolar disorder: preliminary insights from ultra-high field 7T MRSI during task and rest.Frontiers in neuroscience · 2025Article
- Neuroprotective role of lactate in a human in vitro model of the ischemic penumbra.Scientific reports · 2024Article
- Brain sodium sensing for regulation of thirst, salt appetite, and blood pressure.Physiological reports · 2024Review
- Involvement of Astrocytes in the Formation, Maintenance, and Function of the Blood-Brain Barrier.Cells · 2024Review
- Mapping between cognitive theories and psycho-physiological models of attention system performance.Cerebral cortex (New York, N.Y. : 1991) · 2023Review
- Lactate Metabolism, Signaling, and Function in Brain Development, Synaptic Plasticity, Angiogenesis, and Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Lactate: A Theranostic Biomarker for Metabolic Psychiatry?Antioxidants (Basel, Switzerland) · 2023Review
- Astrocyte-neuron lactate shuttle plays a pivotal role in sensory-based neuroprotection in a rat model of permanent middle cerebral artery occlusion.Scientific reports · 2023Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aerobic energy metabolism uses glucose and oxygen to produce all the energy needs of the brain. Several studies published over the last 13 years challenged the assumption that the activated brain increases its oxidative glucose metabolism to meet the increased energy demands. Neuronal function in rat hippocampal slices supplied with 4 mM glucose could tolerate a 15 min activation by a 5 mM concentration of the excitatory neurotransmitter glutamate (Glu), whereas slices supplied with 10 mM glucose could tolerate a 15 min activation by 20 mM Glu. However, in slices in which neuronal lactate use was inhibited by the lactate transporter inhibitor a-cyano-4-hydroxycinnamate (4-CIN), activation by Glu elicited a permanent loss of neuronal function, with a twofold to threefold increase in tissue lactate content. Inhibition of glycolysis with the glucose analog 2-deoxy-D-glucose (2DG) during the period of exposure to Glu diminished normal neuronal function in the majority of slices and significantly reduced the number of slices that exhibited neuronal function after activation. However, when lactate was added with 2DG, the majority of the slices were neuronally functional after activation by Glu. NMDA, a nontransportable Glu analog by the glial glutamate transporter, could not induce a significant increase in slice lactate level when administered in the presence of 4-CIN. It is suggested that the heightened energy demands of activated neurons are met through increased glial glycolytic flux. The lactate thus formed is a crucial aerobic energy substrate that enables neurons to endure activation.
Indexed as
Identifiers
9870935PMC6782362W2111636333What OpenQuestion holds
Registered trials
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.