Abstract
Epilepsy is a chronic neurological disorder manifested by recurring unprovoked seizures resulting from an imbalance in the inhibitory and excitatory neurotransmitters in the brain. The process of epileptogenesis involves a complex interplay between the reduction of inhibitory gamma-aminobutyric acid (GABA) and the enhancement of excitatory glutamate. Pro-BDNF/p75(NTR) expression is augmented in both glial cells and neurons following epileptic seizures and status epileptics (SE). Over-expression of p75(NTR) is linked with the pathogenesis of epilepsy, and augmentation of pro-BDNF/p75(NTR) is implicated in the pathogenesis of epilepsy. However, the precise mechanistic function of p75(NTR) in epilepsy has not been completely elucidated. Therefore, this review aimed to revise the mechanistic pathway of p75(NTR) in epilepsy.