Linked Life Data

12372003

Source:http://linkedlifedata.com/resource/pubmed/id/12372003

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2002-10-9
pubmed:abstractText
The neurotransmitter serotonin (5-HT) stimulates adrenocorticotropic hormone (ACTH) secretion from the anterior pituitary gland via activation of central 5-HT1 and 5-HT2 receptors. The effect of 5-HT is predominantly indirect and may be mediated via release of hypothalamic corticotropin-releasing hormone (CRH). We therefore investigated the possible involvement of CRH in the serotonergic stimulation of ACTH secretion in male rats. Increased neuronal 5-HT content induced by systemic administration of the precursor 5-hydroxytryptophan (5-HTP) in combination with the 5-HT reuptake inhibitor fluoxetine raised CRH mRNA expression in the paraventricular nucleus (PVN) by 64%, increased pro-opiomelanocortin (POMC) mRNA in the anterior pituitary lobe by 17% and stimulated ACTH secretion five-fold. Central administration of 5-HT agonists specific to 5-HT1A, 5-HT1B, 5-HT2A or 5-HT2C receptors increased CRH mRNA in the PVN by 15-50%, POMC mRNA in the anterior pituitary by 15-27% and ACTH secretion three- to five-fold, whereas a specific 5-HT3 agonist had no effect. Systemic administration of a specific anti-CRH antiserum inhibited the ACTH response to 5-HTP and fluoxetine and prevented the 5-HTP and fluoxetine-induced POMC mRNA response in the anterior pituitary lobe. Central or systemic infusion of 5-HT increased ACTH secretion seven- and eight-fold, respectively. Systemic pretreatment with the anti-CRH antiserum reduced the ACTH responses to 5-HT by 80% and 64%, respectively. It is concluded that 5-HT via activation of 5-HT1A, 5-HT2A, 5-HT2C and possibly also 5-HT1B receptors increases the synthesis of CRH in the PVN and POMC in the anterior pituitary lobe, which results in increased ACTH secretion. Furthermore, the results indicate that CRH is an important mediator of the ACTH response to 5-HT.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0953-8194
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
788-95
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12372003-Adrenocorticotropic Hormone, pubmed-meshheading:12372003-Animals, pubmed-meshheading:12372003-Antimetabolites, Antineoplastic, pubmed-meshheading:12372003-Corticotropin-Releasing Hormone, pubmed-meshheading:12372003-Floxuridine, pubmed-meshheading:12372003-Gene Expression, pubmed-meshheading:12372003-Male, pubmed-meshheading:12372003-Paraventricular Hypothalamic Nucleus, pubmed-meshheading:12372003-Pituitary Gland, Anterior, pubmed-meshheading:12372003-Pro-Opiomelanocortin, pubmed-meshheading:12372003-RNA, Messenger, pubmed-meshheading:12372003-Rats, pubmed-meshheading:12372003-Rats, Wistar, pubmed-meshheading:12372003-Receptor, Serotonin, 5-HT1B, pubmed-meshheading:12372003-Receptors, Serotonin, pubmed-meshheading:12372003-Receptors, Serotonin, 5-HT1, pubmed-meshheading:12372003-Serotonin
pubmed:year
2002
pubmed:articleTitle
Serotonergic stimulation of corticotropin-releasing hormone and pro-opiomelanocortin gene expression.
pubmed:affiliation
Department of Medical Physiology, The Panum Institute, University of Copenhagen, Denmark. hsj@mfi.ku.dk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't