Effects of a ketogenic diet on hippocampal plasticity in freely moving juvenile rats

Ketogenic diets are low‐carbohydrate, sufficient protein, high‐fat diets with anticonvulsant activity used primarily as a treatment for pediatric epilepsy. The anticonvulsant mechanism is thought to involve elevating inhibition and/or otherwise limiting excitability in the brain. Such a mechanism, h...

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Bibliographic Details
Published in:Physiological reports 2015-05, Vol.3 (5), p.e12411-n/a
Main Authors: Blaise, J. Harry, Ruskin, David N., Koranda, Jessica L., Masino, Susan A.
Format: Article
Language:English
Subjects:
Alzheimer's disease
Animal cognition
Anticonvulsants
Convulsions & seizures
Dentate gyrus
Diet
Electrodes
Epilepsy
Excitability
High carbohydrate diet
High fat diet
High protein diet
Hippocampal plasticity
Hippocampus
Ketogenesis
ketone bodies
Laboratory animals
long‐term potentiation
Low carbohydrate diet
Low protein diet
Memory
Metabolism
Nutrient deficiency
Original Research
paired pulse ratio
Pediatrics
Physiology
Potentiation
Proteins
Recording equipment
Rodents
Seizures
Surgery
Synaptic plasticity
Synaptic transmission
Weaning
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Summary:Ketogenic diets are low‐carbohydrate, sufficient protein, high‐fat diets with anticonvulsant activity used primarily as a treatment for pediatric epilepsy. The anticonvulsant mechanism is thought to involve elevating inhibition and/or otherwise limiting excitability in the brain. Such a mechanism, however, might also significantly affect normal brain activity and limit synaptic plasticity, effects that would be important to consider in the developing brain. To assess ketogenic diet effects on synaptic transmission and plasticity, electrophysiological recordings were performed at the perforant path/dentate gyrus synapse in awake, freely‐behaving juvenile male rats. Electrodes were implanted 1 week prior to recording. Animals were fed regular chow or a ketogenic diet ad libitum for 3 weeks before recording. Although the ketogenic diet did not significantly alter baseline excitability (assessed by input–output curves) or short‐term plasticity (using the paired‐pulse ratio), it did reduce the magnitude of long‐term potentiation at all poststimulation timepoints out to the last time measured (48 h). The results suggest an effect of ketogenic diet‐feeding on the induction magnitude but not the maintenance of long‐term potentiation. The lack of effect of the diet on baseline transmission and the paired‐pulse ratio suggests a mechanism that limits excitation preferentially in conditions of strong stimulation, consonant with clinical reports in which the ketogenic diet alleviates seizures without a major impact on normal brain activity. Limiting plasticity in a seizure‐susceptible network may limit seizure‐induced epileptogenesis which may subserve the ongoing benefit of the ketogenic diet in epilepsy. We investigated effects of the low carbohydrate, high fat ketogenic diet on dentate gyrus electrophysiology in freely‐moving rats. Three weeks of ketogenic diet feeding diet does not change hippocampal baseline excitability or short‐term (paired pulse) plasticity, but did significantly reduces the magnitude of hippocampal long‐term potentiation measured over 2 days. Antiseizure effects & limitation of long‐term potentiation likely share common mechanisms; however, negative cognitive effects of the diet are rarely found.
ISSN:2051-817X
2051-817X
DOI:10.14814/phy2.12411