Abstract
Antiepileptic drugs (AEDs) represent the mainstay of epilepsy treatment, but we do not yet fully understand the mechanistic basis for their actions. A detailed knowledge of the molecular and cellular effects of AEDs is of paramount importance in our efforts to develop novel compounds with improved efficacy and safety profiles. There are three major classes of molecular targets on neuronal cell membranes believed to be relevant for the clinical actions of AEDs: (1) voltage-gated sodium and calcium channels; (2) γ-aminobutyric acid (GABAA) receptors; and (3) ionotropic glutamate receptors. AEDs exert their effects principally on one or more of these targets.