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James O. McNamara1,2,3*,,
Yang Zhong Huang1,, and
A. Soren Leonard1,
1Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. 2Department of Medicine (Neurology), Duke University Medical Center, Durham, NC 27710, USA. 3Center for Translational Neuroscience, Duke University Medical Center, Durham, NC 27710, USA.
These authors contributed equally to this work.
Gloss: The epilepsies, disorders of recurrent seizures, affect about 1% of the population worldwide. Available therapy is symptomatic in that drugs inhibit seizures but are not disease-modifying; that is, no effective pharmacological prevention or cure has been identified. The term "epileptogenesis" refers to the process by which a normal brain becomes epileptic. Understanding the cellular mechanisms of epileptogenesis in molecular terms may help identify molecular targets for which small-molecule therapeutics can be developed to prevent epileptogenesis in individuals at high risk. A number of acquired and genetic causes of this disorder have been identified, and various in vivo and in vitro models of epileptogenesis have been established. The objective of this STKE Review, with 5 figures, 2 tables, and 199 references, is to review current insights into the molecular signaling mechanisms underlying epileptogenesis, focusing on limbic epileptogenesis in particular.