Depressed glutamate transporter 1 expression in a mouse model of Dravet syndrome

Abstract

AbstractDravet syndrome (DS) is a monogenic, often refractory, epilepsy resultant from SCN1A haploinsufficiency in humans. A novel therapeutic target in DS that can be engaged in isolation or as adjunctive therapy is highly desirable. Here, we demonstrate reduced expression of the rodent glutamate transporter type 1 (GLT‐1) in a DS mouse model, and in wild type mouse strains where Scn1a haploinsufficiency is most likely to cause epilepsy, indicating that GLT‐1 depression may play a role in DS seizures. As GLT‐1 can be upregulated by common and safe FDA‐approved medications, this strategy may be an attractive, viable, and novel avenue for DS treatment.