Febrile seizures: traffic slows in the heat

Abstract

Febrile seizures, which occur in young children, have long been known to have a major inherited component. Mutations in some genes that encode sodium channel and GABAA receptor subunits have been found in a few families affected by febrile seizures. These mutations account only for a minority of cases, and much remains to be learnt about the molecular architecture of febrile seizures. A rare inherited cause - a mutation in the GABAA receptor subunit GABRG2 gene, has been recently shown to cause a temperature-dependent intracellular trafficking defect. This is an important step in unravelling the molecular pathogenesis of this common childhood disorder. © 2006 Elsevier Ltd. All rights reserve..