4E-BP2–dependent translation in parvalbumin neurons controls epileptic seizure threshold

Significance In numerous models of neurodevelopmental disorders and epilepsy, genetic mutations associated with enhanced mTORC1 activity engender an increase in the susceptibility to epileptic seizures. This study shows that deletion mTORC1-downstream translational repressor, 4E-BP2, but not 4E-BP1, promotes epileptogenesis. By deleting 4E-BP2 different cell types, we reveal up-regulation mTORC1/eIF4E signaling parvalbumin inhibitory neurons is sufficient reduce threshold for induction We conclude downstream mTORC1, main 4E-BP paralog controlling epileptogenesis propose are a vulnerable type which aberrant activation mTORC1-dependent translation contributes pathology.