Source:http://linkedlifedata.com/resource/pubmed/id/10098725
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1999-5-6
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pubmed:abstractText |
Increases in the brain concentrations of tryptophan and in serotonin (5-HT) metabolism are commonly observed in animals under stress. Previous experiments indicated that the increase in brain tryptophan and 5-hydroxyindoleacetic acid (5-HIAA) observed in response to administration of endotoxin (lipopolysaccharide, LPS) and interleukin-1 (IL-1) were largely prevented by pretreatment with N-nitro-L-arginine methylester (L-NAME), an inhibitor of NO synthase (NOS). Therefore we tested whether the increases in tryptophan and 5-HT metabolism observed following restraint and footsthock were similarly affected. Mice were injected with L-NAME (30 mg/kg) or saline and restrained for 40 min. Restraint caused increases in concentrations of tryptophan and the catabolites of dopamine (DA), norepinephrine (NE) and 5-HT in the medial prefrontal cortex, hypothalamus, and brain stem. The L-NAME pretreatment significantly attenuated, but did not prevent, the changes in tryptophan and catecholamine metabolism, with a very small effect on the increase in plasma corticosterone. When mice pretreated with L-NAME were subjected to 30 min footshock, the NOS inhibitor had no statistically significant effects on the increases in DA, NE and 5-HT metabolism, but tended to attenuate the increases in tryptophan. We interpret these results to indicate that NOS plays a relatively small role in the cerebral neurochemical responses to restraint and footshock, but the role in the restraint-induced changes was greater than that in the footshock-induced ones. The attenuation of the restraint-related effects on the catecholamines most probably reflects a contribution to the CNS responses from peripheral vascular changes which are likely to be limited by the inhibition of NOS.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Catecholamines,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/NG-Nitroarginine Methyl Ester,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Tryptophan
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0197-0186
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
33
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
551-7
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10098725-Animals,
pubmed-meshheading:10098725-Brain,
pubmed-meshheading:10098725-Catecholamines,
pubmed-meshheading:10098725-Electric Stimulation,
pubmed-meshheading:10098725-Enzyme Inhibitors,
pubmed-meshheading:10098725-Immobilization,
pubmed-meshheading:10098725-Male,
pubmed-meshheading:10098725-Mice,
pubmed-meshheading:10098725-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:10098725-Nitric Oxide Synthase,
pubmed-meshheading:10098725-Tryptophan
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pubmed:year |
1998
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pubmed:articleTitle |
Brain catecholaminergic and tryptophan responses to restraint are attenuated by nitric oxide synthase inhibition.
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pubmed:affiliation |
Department of Pharmacology and Therapeutics, Louisiana State University Medical Center, Shreveport 71130, USA. adunn@lsumc.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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