ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Ketogenic diet metabolites reduce firing in central neurons by opening K(ATP) channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers.
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Who cites it
152 citing papers in PubMed, 289 citations in OpenAlex.
- Cardiovascular Effects of Treatment With the Ketone Body 3-Hydroxybutyrate in Chronic Heart Failure Patients.Circulation · 2019Trial
- Computational Modeling of Neurotransmitter Cycling Predicts Human Brain Glutamate and GABA Dynamics in Response to Acute Administration of Exogenous Ketones.Neurochemical research · 2026Article
- β-Hydroxybutyrate Maintains Energetically Demanding Neural Functions During Exogenous Glucose Deprivation.Cellular and molecular neurobiology · 2026Article
- Article
- Hydroxycarboxylic Acid Receptor 2 Mediates β-hydroxybutyrate's Antiseizure Effect in Mice.Annals of neurology · 2026Article
- Ketogenic diet dampens excitatory neurotransmission by shrinking synaptic vesicle pools.Cell reports · 2026Article
- Mitochondrial membrane junction-mediated ATP channeling drives activity-dependent glucose metabolism.bioRxiv : the preprint server for biology · 2025Article
- Harnessing metabolic control for synaptic stability: REST/NRSF links glycolytic inhibition to excitatory neurotransmission.The Journal of physiology · 2025Article
- Providing alternative fuel for the brain in anorexia nervosa: a review of the literature on ketones and their effects on metabolism and the brain.Translational psychiatry · 2025Review
- Ketone Supplements and Alcohol-Related Responses in Rodents.Addiction biology · 2025Article
- Modulation of pain by ketones: a mini-review.American journal of physiology. Cell physiology · 2025Review
- Fasting and Headache.Current pain and headache reports · 2025Review
- Impact of the Ketogenic Diet on Neurological Diseases: A Review.Life (Basel, Switzerland) · 2025Review
- Acetoacetate, a ketone body, attenuates neuronal bursts in acutely-induced epileptiform slices of the mouse hippocampus.Frontiers in cellular neuroscience · 2025Article
- Exposure to β-hydroxybutyrate reduces the operating set point and increases excitability in hippocampal circuitry of healthy mice.Frontiers in pharmacology · 2025Article
- Neuroglia and brain energy metabolism.Handbook of clinical neurology · 2025Review
- Putative Role of Adenosine A1 Receptors in Exogenous Ketone Supplements-Evoked Anti-Epileptic Effect.International journal of molecular sciences · 2024Review
- Metabolic Reprogramming of Astrocytes in Pathological Conditions: Implications for Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Multi-omics Mendelian randomization integrating GWAS, eQTL and pQTL data revealed GSTM4 as a potential drug target for migraine.The journal of headache and pain · 2024Article
- Characterization of β-Hydroxybutyrate as a Cell Autonomous Fuel for Active Excitatory and Inhibitory Neurons: β-Hydroxybutyrate as a Fuel for Active Neurons.bioRxiv : the preprint server for biology · 2024Article
92 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A low-carbohydrate ketogenic diet remains one of the most effective (but mysterious) treatments for severe pharmacoresistant epilepsy. We have tested for an acute effect of physiological ketone bodies on neuronal firing rates and excitability, to discover possible therapeutic mechanisms of the ketogenic diet. Physiological concentrations of ketone bodies (beta-hydroxybutyrate or acetoacetate) reduced the spontaneous firing rate of neurons in slices from rat or mouse substantia nigra pars reticulata. This region is thought to act as a "seizure gate," controlling seizure generalization. Consistent with an anticonvulsant role, the ketone body effect is larger for cells that fire more rapidly. The effect of ketone bodies was abolished by eliminating the metabolically sensitive K(ATP) channels pharmacologically or by gene knock-out. We propose that ketone bodies or glycolytic restriction treat epilepsy by augmenting a natural activity-limiting function served by K(ATP) channels in neurons.
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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.