RT Journal Article SR Electronic T1 Wortmannin Attenuates Seizure-Induced Hyperactive PI3K/Akt/mTOR Signaling, Impaired Memory, and Spine Dysmorphology in Rats JF eneuro JO eNeuro FD Society for Neuroscience SP ENEURO.0354-16.2017 DO 10.1523/ENEURO.0354-16.2017 VO 4 IS 3 A1 Carter, Angela N. A1 Born, Heather A. A1 Levine, Amber T. A1 Dao, An T. A1 Zhao, Amanda J. A1 Lee, Wai L. A1 Anderson, Anne E. YR 2017 UL http://www.eneuro.org/content/4/3/ENEURO.0354-16.2017.abstract AB Numerous studies have shown epilepsy-associated cognitive deficits, but less is known about the effects of one single generalized seizure. Recent studies demonstrate that a single, self-limited seizure can result in memory deficits and induces hyperactive phosphoinositide 3-kinase/Akt (protein kinase B)/mechanistic target of rapamycin (PI3K/Akt/mTOR) signaling. However, the effect of a single seizure on subcellular structures such as dendritic spines and the role of aberrant PI3K/Akt/mTOR signaling in these seizure-induced changes are unclear. Using the pentylenetetrazole (PTZ) model, we induced a single generalized seizure in rats and: (1) further characterized short- and long-term hippocampal and amygdala-dependent memory deficits, (2) evaluated whether there are changes in dendritic spines, and (3) determined whether inhibiting hyperactive PI3K/Akt/mTOR signaling rescued these alterations. Using the PI3K inhibitor wortmannin (Wort), we partially rescued short- and long-term memory deficits and altered spine morphology. These studies provide evidence that pathological PI3K/Akt/mTOR signaling plays a role in seizure-induced memory deficits as well as aberrant spine morphology.