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SHORT COMMUNICATION Sodium channel β1‐subunit expression is increased in reactive astrocytes in a rat model for mesial temporal lobe epilepsy
Author(s) -
Gorter Jan A.,
Van Vliet Erwin A.,
Da Silva Fernando H. Lopes,
Isom Lori L.,
Aronica Eleonora
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2002.02078.x
Subject(s) - epileptogenesis , epilepsy , sodium channel , neuroscience , hippocampus , neuropil , glial fibrillary acidic protein , gliosis , temporal lobe , protein subunit , biology , chemistry , microbiology and biotechnology , pathology , medicine , immunohistochemistry , sodium , central nervous system , biochemistry , organic chemistry , gene
As several epilepsy syndromes are associated with changes in sodium channel subunits we investigated the expression of β1 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 β1 subunit protein was moderately expressed in neurons and weakly expressed in resting astrocytes. β1 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 β1 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.