The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Ketogenic Diet Metabolites Reduce Firing in Central Neurons by Opening K ATP Channels
Open accessAbstract
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 (β-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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Cites
Membrane Phospholipid Control of Nucleotide Sensitivity of K ATP Channels
Shyng, S.-L., & Nichols, C. G. (1998) · Science · doi:10.1126/science.282.5391.1138 · Cited by 559
KATP channel‐independent targets of diazoxide and 5‐hydroxydecanoate in the heart
Hanley, P. J., Mickel, M., Löffler, M., Brandt, U., & Daut, J. (2002) · The Journal of Physiology · doi:10.1113/jphysiol.2002.023960 · Cited by 320
Sulfonylurea and K+-Channel Opener Sensitivity of KATP Channels
Koster, J. C., Sha, Q., & Nichols, C. G. (1999) · The Journal of General Physiology · doi:10.1085/jgp.114.2.203 · Cited by 97 · cited 2×
“Sulfonylurea sensitivity of KATP channels can vary greatly between different cells expressing identical Kir6 and SUR subtypes and can vary with physiological changes in negatively charged lipids (Koster et al., 1999; Krauter et al., 2001), metabolic stress (Findlay, 1993), reactive oxygen species (Krippeit-Drews et al.”
Cited by
β-Hydroxybutyrate: A Signaling Metabolite
Newman, J. C., & Verdin, E. (2017) · Annual Review of Nutrition · doi:10.1146/annurev-nutr-071816-064916 · Cited by 872
“The nonmetabolized enantiomer S-BHB did not have a similar effect on neuron firing (78); a later study showed that the change in KATP channel opening is due to reduced glycolysis in the presence of BHB (76) and that providing sufficient BHB and oxygen to maintain normal cellular ATP production can prevent the change i…”
Nielsen, R., Møller, N., Gormsen, L. C., Tolbod, L. P., Hansson, N. H., Sorensen, J., Harms, H. J., Frøkiær, J., Eiskjaer, H., Jespersen, N. R., et al. (2019) · Circulation · doi:10.1161/circulationaha.118.036459 · Cited by 518
Jones, L. L., McDonald, D. A., & Borum, P. R. (2010) · Progress in Lipid Research · doi:10.1016/j.plipres.2009.08.004 · Cited by 454
The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders
Stafstrom, C. E., & Rho, J. M. (2012) · Frontiers in Pharmacology · doi:10.3389/fphar.2012.00059 · Cited by 438
Targeting LDH enzymes with a stiripentol analog to treat epilepsy
Sada, N., Lee, S., Katsu, T., Otsuki, T., & Inoue, T. (2015) · Science · doi:10.1126/science.aaa1299 · Cited by 413
Metadata
- Authors
- Ma, W., Berg, J., & Yellen, G.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2007-04-04
- Volume
- 27
- Issue
- 14
- Pages
- 3618-3625
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2037590564
- Cited by
- 294
- References
- 3
- FWCI
- 8.90
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Ma, W., Berg, J., & Yellen, G. (2007). Ketogenic Diet Metabolites Reduce Firing in Central Neurons by Opening K ATP Channels. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0132-07.2007
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
