INCREASED GLUTAMINE-SYNTHETASE IMMUNOREACTIVITY IN EXPERIMENTAL PNEUMOCOCCAL MENINGITIS

Glutamine synthetase (GS), glial fibrillary acidic protein (GFAP) immu nohistochemistry and neuronal apoptotic cell death were evaluated in a rabbit model of pneumococcal meningitis. Meningitis caused an increas e of GS immunoreactivity in the cerebral cortex, but not in the hippoc ampal formation. GFAP immunoreactivity remained unchanged. This may re present 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 durin g meningitis.