Role of nitric oxide in ethanol-induced ascorbic acid release in striatum of freely moving mice

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), Nomega-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.