Source:http://linkedlifedata.com/resource/pubmed/id/17443768
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
|
pubmed:dateCreated |
2007-4-19
|
pubmed:abstractText |
Inductive signals mediating the differentiation of neural precursors into serotonergic (5-HT) or dopaminergic neurons have not been clarified. We have recently shown that in cell aggregates obtained from rat mesencephalic precursors, reduction of serotonin levels induces a marked increase in generation of dopaminergic neurons. In the present study we treated rat neurospheres with antagonists of the main subtypes of 5-HT receptors, 5-HT transport inhibitors, or 5-HT receptor agonists, and studied the effects on generation of dopaminergic neurons. Cultures treated with Methiothepin (5-HT(1,2,5,6,7) receptor antagonist), the 5-HT(4) receptor antagonist GR113808;67:00-.or the 5-HT(7) receptor antagonist SB 269970 showed a significant increase in generation of dopaminergic cells. Treatment with the 5-HT(1B/1D) antagonist GR 127935, the 5-HT(2) antagonist Ritanserin, the 5-HT transporter inhibitor Fluoxetine, the dopamine and norepinephrine transport inhibitor GBR 12935, or with both inhibitors together, or 5-HT(4) or 5-HT(7) receptor agonists induced significant decreases in generation of dopaminergic cells. Cultures treated with WAY100635 (5-HT(1A) receptor antagonist), the 5-HT(3) receptor antagonist Ondasetron, or the 5-HT(6) receptor antagonist SB 258585 did not show any significant changes. Therefore, 5-HT(4) and 5-HT(7) receptors are involved in the observed serotonin-induced decrease in generation of dopaminergic neurons from proliferating neurospheres of mesencephalic precursors. 5-HT(4) and 5-HT(7) receptors were found in astrocytes and serotonergic cells using double immunolabeling and laser confocal microscopy, and the glial receptors appeared to play a major role.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Fluoxetine,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotransmitter Uptake Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Serotonin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Serotonin, 5-HT4,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine 3-Monooxygenase,
http://linkedlifedata.com/resource/pubmed/chemical/serotonin 7 receptor
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jan
|
pubmed:issn |
1932-8451
|
pubmed:author | |
pubmed:copyrightInfo |
(c) 2006 Wiley Periodicals, Inc.
|
pubmed:issnType |
Print
|
pubmed:volume |
67
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
10-22
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:17443768-Animals,
pubmed-meshheading:17443768-Cell Differentiation,
pubmed-meshheading:17443768-Cells, Cultured,
pubmed-meshheading:17443768-Dopamine,
pubmed-meshheading:17443768-Dose-Response Relationship, Drug,
pubmed-meshheading:17443768-Embryo, Mammalian,
pubmed-meshheading:17443768-Fluoxetine,
pubmed-meshheading:17443768-Mesencephalon,
pubmed-meshheading:17443768-Neurons,
pubmed-meshheading:17443768-Neurotransmitter Uptake Inhibitors,
pubmed-meshheading:17443768-Rats,
pubmed-meshheading:17443768-Rats, Sprague-Dawley,
pubmed-meshheading:17443768-Receptors, Serotonin,
pubmed-meshheading:17443768-Receptors, Serotonin, 5-HT4,
pubmed-meshheading:17443768-Serotonin,
pubmed-meshheading:17443768-Serotonin Antagonists,
pubmed-meshheading:17443768-Stem Cells,
pubmed-meshheading:17443768-Tyrosine 3-Monooxygenase
|
pubmed:year |
2007
|
pubmed:articleTitle |
Serotonin decreases generation of dopaminergic neurons from mesencephalic precursors via serotonin type 7 and type 4 receptors.
|
pubmed:affiliation |
Laboratory of Neuroanatomy and Experimental Neurology, Department of Morphological Sciences, Faculty of Medicine, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|