Mitochondrial involvement and oxidative stress in temporal lobe epilepsy

A role for mitochondria and oxidative stress is emerging in acquired epilepsies such as temporal lobe epilepsy (TLE). TLE is characterized by chronic unprovoked seizures arising from an inciting insult with a variable seizure-free "latent period." The mechanism by which inciting injury induces chronic epilepsy, known as epileptogenesis, involves multiple cellular, molecular, and physiological changes resulting in altered hyperexcitable circuitry. Whether mitochondrial and redox mechanisms contribute to epileptogenesis remains to be fully clarified. Mitochondrial impairment is revealed in studies from human imaging and tissue analysis from TLE patients. The collective data from animal models suggest that steady-state mitochondrial reactive oxygen species and resultant oxidative damage to cellular macromolecules occur during different phases of epileptogenesis. This review discusses evidence for the role of mitochondria and redox changes occurring in human and experimental TLE. Potential mechanisms by which mitochondrial energetic and redox mechanisms contribute to increased neuronal excitability and therapeutic approaches to target TLE are delineated.