Source:http://linkedlifedata.com/resource/pubmed/id/20969568
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2010-12-2
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pubmed:abstractText |
The deletion of microtubule-associated protein stable tubule only polypeptide (STOP) leads to neuroanatomical, biochemical and severe behavioral alterations in mice, partly alleviated by antipsychotics. Therefore, STOP knockout (KO) mice have been proposed as a model of some schizophrenia-like symptoms. Preliminary data showed decreased brain serotonin (5-HT) tissue levels in STOP KO mice. As literature data demonstrate various interactions between microtubule-associated proteins and 5-HT, we characterized some features of the serotonergic neurotransmission in STOP KO mice. In the brainstem, mutant mice displayed higher tissue 5-HT levels and in vivo synthesis rate, together with marked increases in 5-HT transporter densities and 5-HT1A autoreceptor levels and electrophysiological sensitivity, without modification of the serotonergic soma number. Conversely, in projection areas, STOP KO mice exhibited lower 5-HT levels and in vivo synthesis rate, associated with severe decreases in 5-HT transporter densities, possibly related to reduced serotonergic terminals. Mutant mice also displayed a deficit of adult hippocampal neurogenesis, probably related to both STOP deletion and 5-HT depletion. Finally, STOP KO mice exhibited a reduced anxiety- and, probably, an increased helpness-status, that could be because of the strong imbalance of the serotonin neurotransmission between somas and terminals. Altogether, these data suggested that STOP deletion elicited peculiar 5-HT disconnectivity.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1471-4159
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pubmed:author |
pubmed-author:AndrieuxAnnieA,
pubmed-author:ChaliFarahF,
pubmed-author:DeloulmeJean-ChristopheJC,
pubmed-author:FabreVéroniqueV,
pubmed-author:FournetVincentV,
pubmed-author:GirosBrunoB,
pubmed-author:HamonMichelM,
pubmed-author:JanyMarionM,
pubmed-author:LanfumeyLaurenceL,
pubmed-author:MartresMarie-PascaleMP,
pubmed-author:MessanviFanyF,
pubmed-author:OrsalDidierD,
pubmed-author:SchweitzerAnnieA
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pubmed:copyrightInfo |
© 2010 The Authors. Journal of Neurochemistry © 2010 International Society for Neurochemistry.
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pubmed:issnType |
Electronic
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pubmed:volume |
115
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1579-94
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pubmed:meshHeading |
pubmed-meshheading:20969568-Animals,
pubmed-meshheading:20969568-Brain,
pubmed-meshheading:20969568-Female,
pubmed-meshheading:20969568-Male,
pubmed-meshheading:20969568-Maze Learning,
pubmed-meshheading:20969568-Mice,
pubmed-meshheading:20969568-Mice, 129 Strain,
pubmed-meshheading:20969568-Mice, Inbred BALB C,
pubmed-meshheading:20969568-Mice, Knockout,
pubmed-meshheading:20969568-Microtubule-Associated Proteins,
pubmed-meshheading:20969568-Nerve Net,
pubmed-meshheading:20969568-Serotonin
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pubmed:year |
2010
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pubmed:articleTitle |
The deletion of the microtubule-associated STOP protein affects the serotonergic mouse brain network.
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pubmed:affiliation |
INSERM UMRS 952, CNRS UMR 7224, Université Pierre et Marie Curie, Paris, France.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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