Developmentally regulated impairment of parvalbumin interneuron synaptic transmission in an experimental model of Dravet syndrome
Keisuke Kaneko, Christopher Brian Currin, Kevin M. Goff, Eric R. Wengert, Ala Somarowthu, Tim P. Vogels, Ethan M. Goldberg
Abstract
mice ≥ P35. Modeling confirms that PV-IN axonal propagation is more sensitive to decreased sodium conductance than spike generation. These results demonstrate dynamic dysfunction in Dravet syndrome: combined abnormalities of PV-IN spike generation and propagation drives early disease severity, while ongoing dysfunction of synaptic transmission contributes to chronic pathology.
Topics & Concepts
Dravet syndromeParvalbuminNeuroscienceInterneuronEpilepsyNeurotransmissionSodium channelGABAergicBiologySomaMedicineReceptorGeneticsChemistrySodiumInhibitory postsynaptic potentialOrganic chemistryNeuroscience and Neuropharmacology ResearchIon channel regulation and functionEpilepsy research and treatment