Abstract：
:Removal of glutamate from the synaptic cleft by astroglial glutamine synthase (GS) is a crucial step in the regulation of glutamate turnover and metabolism, thus participating in endogenous neuroprotective processes occurring within brain tissues. Here we investigated on the effect of inflammatory cytokines on GS activity in astroglial cells undergoing NMDA receptors stimulation. Incubation of human cultured astroglial cells with NMDA (100 microM) enhanced GS expression, an effect driven by the generation of nitric oxide (NO) since l-NAME (500 microM), an inhibitor of NO synthase, reversed this effect. NMDA-related increase of GS activity and glutamine concentration was antagonised by previous incubation of astroglial cells with a mixture of LPS plus gammaIFN, an effect counteracted by dexamethasone, the latter effect being accompanied by inhibition of inducible NO synthase. These results show that LPS plus gammaIFN inhibit elevation of GS activity subsequent to NMDA receptor stimulation in astroglial cells via enhancement of inducible NO synthase, and this may represent the site of interaction between pro-inflammatory and excitotoxic stimuli in the brain.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Muscoli C,Visalli V,Colica C,Nisticò R,Palma E,Costa N,Rotiroti D,Nisticò G,Mollace Vdoi
10.1016/j.neulet.2004.09.079keywords:
subject
Has Abstractpub_date
2005-01-20 00:00:00pages
184-8issue
3eissn
0304-3940issn
1872-7972pii
S0304-3940(04)01312-6journal_volume
373pub_type
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