The gamma-butyrolactone model of absence epilepsy: Acute and chronic effects in wistar rats

Abstract

Introduction A pharmacological modeling approach to absence epilepsy requires a reproducible and predictable method that has the EEG and behavioral characteristics of generalized typical absence seizures in humans. The gamma-hydroxybutyrate (GHB) and gamma-butryrolactone (GBL) models meets these criteria.[1,2] The acute administration of GBL, which is a prodrug of GHB, has been shown to produce exactly the same EEG and behavioral effects of absence seizures as GHB [3] and GBL administration mimics typical absence epilepsy in humans.[4] GBL is preferred due to the consistency, predictable dose response and rapidity of the onset of its action in rodents.[5-7] The systemic administration of a single dose of GBL produces absence seizures through the potentiation of the GHB-related neuromodulation and/or interaction with GABAergic inhibitory and excitatory neurotransmission in the cortico-thalamo-cortical circuit. The objective of this study was to determine the EEG and behavioral changes induced by acute and chronic administration of GBL in male adult Wistar rats