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© 2016 Wayne N. Frankel. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License. Epilepsy is a neurological disorder that is characterized by periodic seizures in affected individuals. The cellular mechanisms during a seizure entail synchronous but abnormal firing of neural networks in the higher centers of the brain. Very early studies on cellular mechanisms of epilepsy especially focused on inducing seizures in animal models by blocking synaptic activity using drugs that either block inhibitory neural networks1 or activate voltage gated channels2 to increase excitation. Many of a growing number of genetically solved epilepsies and their respective animal models have also shown or presume that defective inhibition (leading to excessive excitation) is at the heart of the pathophysiology. In a recent issue of Neurobiology of Disease, Asinof and colleagues stir the pot further with new data in a mouse model of a relatively new and severe form of human epilepsy – DNM1 (dynamin 1) epileptic encephalopathy (EE).

Commentary: "Dynamin 1 isoform roles in a mouse model of severe childhood epileptic encephalopathy"