Sodium channel beta1-subunit expression is increased in reactive astrocytes in a rat model for mesial temporal lobe epilepsy.

Abstract

As several epilepsy syndromes are associated with changes in sodium channel subunits we investigated the expression of beta1 sodium channel protein in a rat epilepsy model. In this model a chronic epileptic syndrome develops after electrically induced status epilepticus (SE). Many neuropathological characteristics of mesial temporal lobe epilepsy can be reproduced (cell loss, gliosis and synaptic reorganization). In control hippocampus beta1 subunit protein was moderately expressed in neurons and weakly expressed in resting astrocytes. beta1 sodium channel immunoreactivity increased markedly within 1 week after SE mainly in astrocytes that were colocalized with vimentin (marker for reactive astrocytes). This up-regulation was still present in reactive astrocytes of chronic epileptic rats (> 3 months after SE). Considering the fact that the beta1 subunits may function as cell adhesion molecules interacting with extracellular matrix, the observed increase in reactive astrocytes might subserve a function in cellular and synaptic reorganization during epileptogenesis.