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Research Article Free access | 10.1172/JCI1009

beta-Hydroxybutyrate fuels synaptic function during development. Histological and physiological evidence in rat hippocampal slices.

Y Izumi, K Ishii, H Katsuki, A M Benz, and C F Zorumski

Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA. izumiy@psychiatry.wustl.edu

Find articles by Izumi, Y. in: JCI | PubMed | Google Scholar

Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA. izumiy@psychiatry.wustl.edu

Find articles by Ishii, K. in: JCI | PubMed | Google Scholar

Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA. izumiy@psychiatry.wustl.edu

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Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA. izumiy@psychiatry.wustl.edu

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Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA. izumiy@psychiatry.wustl.edu

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Published March 1, 1998 - More info

Published in Volume 101, Issue 5 on March 1, 1998
J Clin Invest. 1998;101(5):1121–1132. https://doi.org/10.1172/JCI1009.
© 1998 The American Society for Clinical Investigation
Published March 1, 1998 - Version history
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Abstract

To determine whether ketone bodies sustain neuronal function as energy substrates, we examined the effects of beta-hydroxybutyrate (betaHB) on synaptic transmission and morphological integrity during glucose deprivation in rat hippocampal slices. After the depression of excitatory postsynaptic potentials (EPSPs) by 60 min of glucose deprivation, administration of 0.5-10 mM D-betaHB restored EPSPs in slices from postnatal day (PND) 15 rats but not in slices from PND 30 or 120 rats. At PND 15, adding D-betaHB to the media allowed robust long-term potentiation of EPSPs triggered by high frequency stimulation, and prevented the EPSP-spike facilitation that suggests hyperexcitability of neurons. Even after PND 15,D-betaHB blocked morphological changes produced by either glucose deprivation or glycolytic inhibition. These results indicate that D-betaHB is not only able to substitute for glucose as an energy substrate but is also able to preserve neuronal integrity and stability, particularly during early development.

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