Linked Life Data

12962975

Source:http://linkedlifedata.com/resource/pubmed/id/12962975

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-9-9
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Arginine, http://linkedlifedata.com/resource/pubmed/chemical/Ascorbic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Central Nervous System Depressants, http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Ethanol, http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid, http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Donors, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type I, http://linkedlifedata.com/resource/pubmed/chemical/Nitroprusside, http://linkedlifedata.com/resource/pubmed/chemical/Nos1 protein, mouse
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0378-4274
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
145
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
69-78
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Role of nitric oxide in ethanol-induced ascorbic acid release in striatum of freely moving mice.
pubmed:affiliation
Department of Pharmacology, Shenyang Pharmaceutical University, 110016 Shenyang, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't