Enhanced in vitro CA1 network activity in a sodium channel β1(C121W) subunit model of genetic epilepsy

Abstract

Objective A NaVβ1(C121W) mouse model of human genetic epilepsy has enhanced neuronal excitability and temperature sensitivity attributed to a decreased threshold for action potential firing in the axon initial segment. To investigate the network consequences of this neuronal dysfunction and to establish a genetic disease state model we developed an in vitro assay to investigate CA1 network properties and antiepileptic drug sensitivity. Methods CA1 network oscillations were induced by tetanic stimulation and average number of spikes, interspike interval (ISI), duration, and latency were measured in slices from control and NaVβ 1(C121W) heterozygous mice in the presence and absence of retigabi..