title: Increased glutamine synthetase immunoreactivity in experimental pneumococcal meningitis.
abstract: Glutamine synthetase (GS), glial fibrillary acidic protein (GFAP) immunohistochemistry and neuronal apoptotic cell death were evaluated in a rabbit model of pneumococcal meningitis. Meningitis caused an increase of GS immunoreactivity in the cerebral cortex, but not in the hippocampal formation. GFAP immunoreactivity remained unchanged. This may represent a protective mechanism for cortical neurons. The inability of hippocampal GS to counteract the detrimental effects of glutamate may be the cause of neural apoptosis observed in the dentate gyrus during meningitis.
authors.affiliation: Department of Neurology, Georg-August-University, Göttingen, Germany.
authors.forename: A K
authors.initials: AK
authors.lastname: Stringaris
authors.forename: W
authors.initials: W
authors.lastname: Brück
authors.forename: H
authors.initials: H
authors.lastname: Tumani
authors.forename: H
authors.initials: H
authors.lastname: Schmidt
authors.forename: R
authors.initials: R
authors.lastname: Nau
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism; D004195:Disease Models, Animal; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism; D007150:Immunohistochemistry; D008586:Meningitis, Pneumococcal / Q000378:metabolism*; D011817:Rabbits
chemical_list: D005974:Glutamate-Ammonia Ligase