Journal
EPILEPSY RESEARCH
Volume 95, Issue 1-2, Pages 100-109Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.eplepsyres.2011.03.003
Keywords
Neonate; Ketogenic diet; Seizure; GABA
Categories
Funding
- EU (EC) [LSH-CT-2006-037315 (EPICURE) FP6]
- INSERM
- ANR
- FRM
- LFCE
- Rothschild/Inserm interface programs
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Physiological ketosis is a hallmark of metabolism in suckling infants. However, little is known on the impact of physiological ketosis on brain excitability. We addressed this question in suckling rats in vivo. 16-channel extracellular field potential recordings were performed from somatosensory barrel cortex at postnatal days 5-9 non-anaesthetized rat pups. Seizures were induced by the volatile convulsant agent flurothyl. One hour after blockade of physiological ketogenesis using combined administration of beta-oxidation inhibitors mercaptoacetate, insulin and glucose to prevent hypoglycemia, we found no significant change in the flurothyl-induced electrographic seizures. However, build-up of seizures during two repetitive flurothyl applications was strongly aggravated in the animals with blocked ketogenesis. The effect of ketogenesis inhibitors was reversed by exogenous beta-hydroxybutyrate. Diazepam exerted anticonvulsive action both under physiological ketosis and after blockade of ketogenesis, and bumetanide had no significant anticonvulsive effects in both conditions. Thus, physiological ketosis reduces excitability in the immature brain and elimination of physiological ketosis results in elimination of this anticonvulsant effect. Our study raises concern that the changes in diet, and pharmacological manipulations such as glucose infusion, and pathologies such as hyperinsulinism which break natural ketosis, may be a potential risk factor for epileptogenesis in nursing infants. (c) 2011 Elsevier B.V. All rights reserved.
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