In recent years, oxidative stress and excessive reactive oxygen species (ROS) production have been implicated in many neurological pathologies. Excessive ROS generation during and after seizures have been shown to play a crucial role in immediate and longer-term excitotoxic neuronal death in which it is produced by several sources. Previous studies have shown that mitochondria and ROS producing enzymes, such as NADPH oxidase (NOX), are the main intracellular sources of ROS.

Therefore, we here propose to investigate the temporal profile and cellular localization of the NOX isoforms in normal brain, as well as brains subjected to acute and prolonged (i.e. status epilepticus) models.