We find that the seizure-induced memory impairments are transient and are linked, in part, to dysregulated signaling of a memory related cascade [phosphoinositide 3-kinase/Akt (protein kinase B)/mechanistic target of rapamycin (PI3K/Akt/mTOR)] and possibly also disruptions in spine morphology, both of which are crucial for memory formation. Here, AKT1 is linked to memory impairment.