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Summary
It has been assumed that anticonvulsants or antiepileptic drugs, now called antiseizure drugs (ASDs), act on the underpinnings of nerve cell firing: ion channels that generate action potentials, or neurotransmitter receptors that control synaptic transmission. The breakthroughs heralded by the first generation of ASDs, such as the GABAA (γ-aminobutyric acid type A) receptor modulator phenobarbital and the sodium channel antagonist phenytoin, are a major reason for this view. The emergence of second- and third-generation ASDs that also inhibit ion channels provided additional support. However, as epilepsy research has matured, our understanding of ASDs has also. The report by Sada et al. (1) on page 1362 of this issue exemplifies this trend. The study raises a surprising question: Should the focal point of ASD development actually be neurons?
