Induction of sodium channel Nax (SCN7A) expression in rat and human hippocampus in temporal lobe epilepsy

In a recent large-scale gene-expression study in a rat model of temporal lobe epilepsy (TLE) a persistent up-regulation in the expression of the SCN7A gene was revealed. The SCN7A gene encodes an atypical sodium channel (Na(x) ), which is involved in osmoregulation via a sensing mechanism for the extracellular sodium concentration. Herein we investigated the expression and cellular distribution of SCN7A mRNA and protein in normal and epileptic rat and human hippocampus.SCN7A/Na(x) expression analysis was performed by polymerase chain reaction (PCR), immunocytochemistry, and western blot analysis.Increased expression of SCN7A/Na(x) mRNA/protein was observed during epileptogenesis and in the chronic epileptic phase in the post-status epilepticus (SE) model of TLE. The up-regulation was confirmed in human hippocampal tissue resected from pharmacoresistant patients with hippocampal sclerosis (HS). In both epileptic rat and human hippocampus, increased Na(x) expression was observed in neurons and reactive astrocytes compared to control tissue.The increased and persistent expression of SCN7A/Na(x) in the epileptic rat and human hippocampus supports the possible involvement of this channel in the complex reorganization occurring within the hippocampus during the epileptogenic process in TLE. Further studies are needed for a complete understanding of the functional role of SCN7A in epilepsy.