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Redistribution of astrocytic glutamine synthetase in the hippocampus of chronic epileptic rats
Author(s) -
Papageorgiou Ismini E.,
Gabriel Siegrun,
Fetani Andriani F.,
Kann Oliver,
Heinemann Uwe
Publication year - 2011
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.21217
Subject(s) - glutamine synthetase , epileptogenesis , biology , glutamate receptor , excitotoxicity , hippocampal formation , epilepsy , hippocampus , astrocyte , endocrinology , pilocarpine , medicine , glial fibrillary acidic protein , glutamine , neuroscience , central nervous system , biochemistry , immunohistochemistry , receptor , immunology , amino acid
Glutamine synthetase (GS) is an astrocytic enzyme, which catalyzes the synthesis of glutamine from glutamate and ammonia. In the central nervous system, GS prevents glutamate‐dependent excitotoxicity and detoxifies nitrogen. Reduction in both expression and activity of GS was reported in the hippocampus of patients with temporal lobe epilepsy (TLE), and this reduction has been suggested to contribute to epileptogenesis. In this study, we characterized hippocampal GS expression in the pilocarpine model of TLE in Wistar rats by means of stereology and morphometric analysis. Neither the GS positive cell number nor the GS containing cell volume was found to be altered in different hippocampal subregions of chronic epileptic rats when compared with controls. Instead, redistribution of the enzyme at both intracellular and tissue levels was observed in the epileptic hippocampus; GS was expressed more in proximal astrocytic branches, and GS expressing astrocytic somata was located in closer proximity to vascular walls. These effects were not due to shrinkage of astrocytic processes, as revealed by glial fibrillary acidic protein staining. Our results argue for GS redistribution rather than downregulation in the rat pilocarpine model of TLE. The potential contribution of increased GS perivascular affinity to the pathogenesis of epilepsy is discussed as well. © 2011 Wiley‐Liss, Inc.