Increased glutamine synthetase immunoreactivity in experimental pneumococcal meningitis

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. GFA...

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Veröffentlicht in:Acta neuropathologica 1997-03, Vol.93 (3), p.215-218
Hauptverfasser: STRINGARIS, A. K, BRÜCK, W, TUMANI, H, SCHMIDT, H, NAU, R
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creator STRINGARIS, A. K
BRÜCK, W
TUMANI, H
SCHMIDT, H
NAU, R
description 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.
doi_str_mv 10.1007/s004010050606
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subjects Animals
Apoptosis
Bacterial diseases
Biological and medical sciences
Cell death
Cerebral cortex
Cerebral Cortex - metabolism
Dentate gyrus
Disease Models, Animal
Experimental bacterial diseases and models
Glial fibrillary acidic protein
Glutamate-ammonia ligase
Glutamate-Ammonia Ligase - metabolism
Glutamine
Hippocampus
Hippocampus - metabolism
Immunohistochemistry
Infectious diseases
Medical sciences
Meningitis
Meningitis, Pneumococcal - metabolism
Neuronal-glial interactions
Rabbits
Streptococcus infections
title Increased glutamine synthetase immunoreactivity in experimental pneumococcal meningitis
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