Journal article

Aggravation of absence seizures by carbamazepine in a genetic rat model does not induce neuronal c-Fos activation

C Wallengren, S Li, MJ Morris, B Jupp, TJ O'Brien

Clinical Neuropharmacology | LIPPINCOTT WILLIAMS & WILKINS | Published : 2005

Abstract

The mechanisms underlying carbamazepine aggravation of absence seizures are uncertain but are thought to involve enhancement of neuronal activity within the thalamocortical circuitry. We used c-Fos immunohistochemistry (cFos-ir) to examine patterns of neuronal activation and the relationship to seizure expression following administration of carbamazepine in a rat model of absence epilepsy (Genetic Absence Epilepsy Rats of Strasbourg, GAERS). Female ovariectomized GAERS implanted with extradural EEG electrodes received either 20 mg/kg carbamazepine or vehicle IP. Seizure expression was quantified by measuring the total number and duration of spike-wave discharges (SWD) and with the individual..

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