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.
Yan
Pei Gang
PG
Department of Pharmacology, Shenyang Pharmaceutical University, 110016 Shenyang, PR China.
Wu
Chun Fu
CF
Huang
Mei
M
Liu
Wen
W
D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001205:Ascorbic Acid / Q000378:metabolism*; D002492:Central Nervous System Depressants / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D000431:Ethanol / Q000494:pharmacology*; D005110:Extracellular Space / Q000187:drug effects / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D008297:Male; D051379:Mice; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D017072:Neostriatum / Q000187:drug effects / Q000378:metabolism*; D009569:Nitric Oxide / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052248:Nitric Oxide Synthase Type I; D009599:Nitroprusside / Q000494:pharmacology
D002492:Central Nervous System Depressants; D004791:Enzyme Inhibitors; D020030:Nitric Oxide Donors; D009599:Nitroprusside; D009569:Nitric Oxide; D000431:Ethanol; D018698:Glutamic Acid; D001120:Arginine; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496321:Nos1 protein, mouse; D001205:Ascorbic Acid; D019331:NG-Nitroarginine Methyl Ester