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 neuronal apoptosis observed in the dentate gyrus during meningitis.
Original language | English |
---|---|
Pages (from-to) | 215 - 218 |
Number of pages | 4 |
Journal | Acta Neuropathologica |
Volume | 93 |
Issue number | 3 |
DOIs | |
Publication status | Published - Mar 1997 |