Dexamethasone ameliorates the damage of hippocampal filamentous actin cytoskeleton but is not sufficient to cease epileptogenesis in pilocarpine induced epileptic mice

Abstract

Progressive deconstruction of filament actin (F-actin) in hippocampal neurons in the epileptic brain have
been associated with epileptogenesis. Previous clinical studies suggest that glucocorticoids treatment plays
beneficial roles in refractory epilepsy. Glucocorticoids treatment affects dendritic spine morphology by
regulating local glucocorticoid receptors and F-actin cytoskeleton dynamics.
In the present study, effects of dexamethasone on actin filament organization are examined in a pilocarpineinduced
epileptic model. After treatment with dexamethasone F-actin damage was reduced dramatically
in pilocarpine epileptic mice models. Treatment of dexamethasone is beneficial for reducing neuronal loss
and maintaining synaptic structures. Dexamethasone treatment improves but is not sufficient to cease
epileptogenesis..