The glucocorticoid receptor specific modulator CORT108297 reduces brain pathology following status epilepticus.

Objective: Glucocorticoid levels rise rapidly following status epilepticus and remain elevated for weeks after the injury. To determine whether glucocorticoid receptor activation contributes to the pathological sequelae of status epilepticus, mice were treated with a novel glucocorticoid receptor modulator, C108297.

Methods: Mice were treated with either C108297 or vehicle for 10 days beginning one day after pilocarpine-induced status epilepticus.

Self-reinforcing effects of mTOR hyperactive neurons on dendritic growth.

Loss of the mTOR pathway negative regulator PTEN from hippocampal dentate granule cells leads to neuronal hypertrophy, increased dendritic branching and aberrant basal dendrite formation in animal models. Similar changes are evident in humans with mTOR pathway mutations. These genetic conditions are associated with autism, cognitive dysfunction and epilepsy.

PTEN deletion increases hippocampal granule cell excitability in male and female mice.

Unlabelled: Deletion of the mTOR pathway inhibitor PTEN from postnatally-generated hippocampal dentate granule cells causes epilepsy. Here, we conducted field potential, whole cell recording and single cell morphology studies to begin to elucidate the mechanisms by which granule cell-specific PTEN-loss produces disease. Cells from both male and female mice were recorded to identify sex-specific effects.