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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
1998-8-3
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pubmed:abstractText |
D-Fenfluramine is a serotonin (5-hydroxytryptamine, 5-HT) releaser and reuptake inhibitor. It is used to study the neurochemical control of feeding and has been used to treat obesity. It has also been employed as a pharmacological tool to study changes in serotonergic function in psychiatric patients. Brain sites activated by D-fenfluramine via the release of 5-HT have been mapped via the expression of the immediate early gene c-fos. Studies in our laboratory have indicated that D-fenfluramine induces Fos in the hypothalamus and cortex through 5-HT release. The present study investigated whether 5-HT released by D-fenfluramine induces Fos expression in the brain by activating 5-HT1A or 5-HT2A/2C receptors. Rats were pretreated either with WAY-100635, a 5-HT1A antagonist, or ritanserin, a 5-HT2A/2C antagonist, prior to d-fenfluramine injection. Blockade of either 5-HT1A or 5-HT2A/2C receptors was not sufficient to suppress the Fos response to D-fenfluramine in any region of the brain examined, including the cingulate cortex, frontal cortex, caudate-putamen, paraventricular nucleus of the hypothalamus, amygdala, and brainstem. These results indicate that Fos response elicited by D-fenfluramine may be mediated by other receptors, in addition to the 5-HT1A or 5-HT2A/2C receptors.
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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/Fenfluramine,
http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Piperazines,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-fos,
http://linkedlifedata.com/resource/pubmed/chemical/Pyridines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Serotonin,
http://linkedlifedata.com/resource/pubmed/chemical/Ritanserin,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin Uptake Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/WAY 100635
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 1998 Elsevier Science B.V.
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pubmed:issnType |
Print
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pubmed:day |
27
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pubmed:volume |
791
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
67-74
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9593827-Animals,
pubmed-meshheading:9593827-Brain,
pubmed-meshheading:9593827-Fenfluramine,
pubmed-meshheading:9593827-Male,
pubmed-meshheading:9593827-Nerve Tissue Proteins,
pubmed-meshheading:9593827-Piperazines,
pubmed-meshheading:9593827-Proto-Oncogene Proteins c-fos,
pubmed-meshheading:9593827-Pyridines,
pubmed-meshheading:9593827-Rats,
pubmed-meshheading:9593827-Rats, Sprague-Dawley,
pubmed-meshheading:9593827-Receptors, Serotonin,
pubmed-meshheading:9593827-Ritanserin,
pubmed-meshheading:9593827-Serotonin Antagonists,
pubmed-meshheading:9593827-Serotonin Uptake Inhibitors
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pubmed:year |
1998
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pubmed:articleTitle |
The 5-HT1A and 5-HT2A/2C receptor antagonists WAY-100635 and ritanserin do not attenuate D-fenfluramine-induced fos expression in the brain.
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pubmed:affiliation |
Neuroscience Program, Loyola University of Chicago School of Medicine, Maywood, IL 60153, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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