Abstract
In the present study, in vivo brain microdialysis coupled with high performance liquid chromatography (HPLC) and electrochemical detection were used to evaluate the effects of either l-arginine ( l-Arg), the substrate of nitric oxide synthase (NOS), Nω-nitro- l-arginine methyl ester hydrochloride ( l-NAME), a non-selective NOS inhibitor, or sodium nitroprusside (SNP), a donor of NO, on the ethanol-induced release of ascorbic acid (AA) in the striatum of freely moving mice. Drugs were administered intrastriatally via the microdialysis probe and ethanol (2–4 g/kg) was administered intraperitoneally. The results showed that l-arginine (1–10 mg/ml) had no effect on either the basal AA contents in striatal extracellular fluid or the ethanol-induced release of AA. l-NAME (10 −4 to 10 −3 mg/ml) and SNP (10 −4 to 10 −3 mg/ml) both reduced the basal AA concentrations in striatal extracellular fluid. l-NAME significantly inhibited ethanol-induced release of AA, while SNP only had a transient inhibitory effect on the ethanol-induced release of AA. SNP significantly increased dehydroascorbic acid (DHAA) contents and DHAA/AA ratio but had no effect on the total AA contents (AA and DHAA contents) in striatal extracellular fluid, while l-NAME had no effect on DHAA contents but decreased the total AA contents in striatal extracellular fluid. Only high concentration l-NAME induced a transient increase in DHAA/AA ratio. Our results suggest that nitric oxide (NO) might not directly be involved in the mechanism of ethanol-induced release of AA in mouse striatum.
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