Abstract
The role of glial cells in nitric oxide production in the cerebellum of conscious rats was investigated with a glial selective metabolic inhibitor, fluorocitrate. The levels of nitric oxide metabolites (nitrite plus nitrate) in the dialysate following in vivo microdialysis progressively increased to more than 2-fold the basal levels during a 2-h infusion of fluorocitrate (1 mM), and the increase persisted for more than 2 h after the treatment. Pretreatment with N(G)-nitro-L-arginine methyl ester attenuated the fluorocitrate-induced increase in nitric oxide metabolite levels. None of the glutamate receptor antagonists, including D(-)-2-amino-5-phosphonopentanoic acid, 6,7-dinitroquinoxaline-2,3-dione, and (±)-α-methyl-4- carboxyphenylglycine, inhibited the fluorocitrate-induced increase. The L- arginine-induced increase was significantly reduced by fluorocitrate treatment, while N-methyl-D-aspartate, (+)-α-amino-3-hydroxy-5- methylisoxazole-4-propionic acid, and trans-(±)-1-amino-(1S,3R)- cyclopentane-dicarboxylic acid increased nitric oxide metabolites levels in the fluorocitrate-treated rats, as much as in control animals. These results suggest that glial cells play an important role in modulating nitric oxide production in the cerebellum by regulating L-arginine availability.
Original language | English |
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Pages (from-to) | 72-78 |
Number of pages | 7 |
Journal | Brain Research |
Volume | 762 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 11-07-1997 |
Externally published | Yes |
All Science Journal Classification (ASJC) codes
- Neuroscience(all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology