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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Functional Interaction between Trace Amine-Associated Receptor 1 and Dopamine D2 Receptor</title><author><name sortKey="Espinoza, Stefano" sort="Espinoza, Stefano" uniqKey="Espinoza S" first="Stefano" last="Espinoza">Stefano Espinoza</name></author><author><name sortKey="Salahpour, Ali" sort="Salahpour, Ali" uniqKey="Salahpour A" first="Ali" last="Salahpour">Ali Salahpour</name></author><author><name sortKey="Masri, Bernard" sort="Masri, Bernard" uniqKey="Masri B" first="Bernard" last="Masri">Bernard Masri</name></author><author><name sortKey="Sotnikova, Tatyana D" sort="Sotnikova, Tatyana D" uniqKey="Sotnikova T" first="Tatyana D." last="Sotnikova">Tatyana D. Sotnikova</name></author><author><name sortKey="Messa, Mirko" sort="Messa, Mirko" uniqKey="Messa M" first="Mirko" last="Messa">Mirko Messa</name></author><author><name sortKey="Barak, Larry S" sort="Barak, Larry S" uniqKey="Barak L" first="Larry S." last="Barak">Larry S. Barak</name></author><author><name sortKey="Caron, Marc G" sort="Caron, Marc G" uniqKey="Caron M" first="Marc G." last="Caron">Marc G. Caron</name></author><author><name sortKey="Gainetdinov, Raul R" sort="Gainetdinov, Raul R" uniqKey="Gainetdinov R" first="Raul R." last="Gainetdinov">Raul R. Gainetdinov</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21670104</idno><idno type="pmc">3164335</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3164335</idno><idno type="RBID">PMC:3164335</idno><idno type="doi">10.1124/mol.111.073304</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">000514</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000514</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Functional Interaction between Trace Amine-Associated Receptor 1 and Dopamine D2 Receptor</title><author><name sortKey="Espinoza, Stefano" sort="Espinoza, Stefano" uniqKey="Espinoza S" first="Stefano" last="Espinoza">Stefano Espinoza</name></author><author><name sortKey="Salahpour, Ali" sort="Salahpour, Ali" uniqKey="Salahpour A" first="Ali" last="Salahpour">Ali Salahpour</name></author><author><name sortKey="Masri, Bernard" sort="Masri, Bernard" uniqKey="Masri B" first="Bernard" last="Masri">Bernard Masri</name></author><author><name sortKey="Sotnikova, Tatyana D" sort="Sotnikova, Tatyana D" uniqKey="Sotnikova T" first="Tatyana D." last="Sotnikova">Tatyana D. Sotnikova</name></author><author><name sortKey="Messa, Mirko" sort="Messa, Mirko" uniqKey="Messa M" first="Mirko" last="Messa">Mirko Messa</name></author><author><name sortKey="Barak, Larry S" sort="Barak, Larry S" uniqKey="Barak L" first="Larry S." last="Barak">Larry S. Barak</name></author><author><name sortKey="Caron, Marc G" sort="Caron, Marc G" uniqKey="Caron M" first="Marc G." last="Caron">Marc G. Caron</name></author><author><name sortKey="Gainetdinov, Raul R" sort="Gainetdinov, Raul R" uniqKey="Gainetdinov R" first="Raul R." last="Gainetdinov">Raul R. Gainetdinov</name></author></analytic><series><title level="j">Molecular Pharmacology</title><idno type="ISSN">0026-895X</idno><idno type="eISSN">1521-0111</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The ability of dopamine receptors to interact with other receptor subtypes may provide mechanisms for modulating dopamine-related functions and behaviors. In particular, there is evidence suggesting that the trace amine-associated receptor 1 (TAAR1) affects the dopaminergic system by regulating the firing rate of dopaminergic neurons or by altering dopamine D2 receptor (D2R) responsiveness to ligands. TAAR1 is a Gα<sub>s</sub> protein-coupled receptor that is activated by biogenic amines, “trace amines,” such as β-phenylethylamine (β-PEA) and tyramine that are normally found at low concentrations in the mammalian brain. In the present study, we investigated the biochemical mechanism of interaction between TAAR1 and D2R and the role this interaction plays in D2R-related signaling and behaviors. Using a bioluminescence resonance energy transfer biosensor for cAMP, we demonstrated that the D2R antagonists haloperidol, raclopride, and amisulpride were able to enhance selectively a TAAR1-mediated β-PEA increase of cAMP. Moreover, TAAR1 and D2R were able to form heterodimers when coexpressed in human embryonic kidney 293 cells, and this direct interaction was disrupted in the presence of haloperidol. In addition, in mice lacking TAAR1, haloperidol-induced striatal c-Fos expression and catalepsy were significantly reduced. Taken together, these data suggest that TAAR1 and D2R have functional and physical interactions that could be critical for the modulation of the dopaminergic system by TAAR1 in vivo.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Mol Pharmacol</journal-id><journal-id journal-id-type="hwp">molpharm</journal-id><journal-id journal-id-type="pmc">molpharm</journal-id><journal-id journal-id-type="publisher-id">MolPharm</journal-id><journal-title-group><journal-title>Molecular Pharmacology</journal-title></journal-title-group><issn pub-type="ppub">0026-895X</issn><issn pub-type="epub">1521-0111</issn><publisher><publisher-name>The American Society for Pharmacology and Experimental Therapeutics</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">21670104</article-id><article-id pub-id-type="pmc">3164335</article-id><article-id pub-id-type="publisher-id">3710660</article-id><article-id pub-id-type="doi">10.1124/mol.111.073304</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>Functional Interaction between Trace Amine-Associated Receptor 1 and Dopamine D2 Receptor</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Espinoza</surname><given-names>Stefano</given-names></name></contrib><contrib contrib-type="author"><name><surname>Salahpour</surname><given-names>Ali</given-names></name></contrib><contrib contrib-type="author"><name><surname>Masri</surname><given-names>Bernard</given-names></name></contrib><contrib contrib-type="author"><name><surname>Sotnikova</surname><given-names>Tatyana D.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Messa</surname><given-names>Mirko</given-names></name></contrib><contrib contrib-type="author"><name><surname>Barak</surname><given-names>Larry S.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Caron</surname><given-names>Marc G.</given-names></name></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Gainetdinov</surname><given-names>Raul R.</given-names></name></contrib><aff>Department of Neuroscience and Brain Technologies, Italian Institute of Technology, Genoa, Italy (S.E., R.R.G., T.D.S.); Department of Cell Biology, Duke University, Durham, North Carolina (L.S.B., M.G.C., R.R.G.); Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada (A.S.); Institut National de la Santé et de la Recherche Médicale Unité Mixte de Recherche 1037, Cancer Research Center of Toulouse and Université de Toulouse III, UPS, Toulouse, France (B.M.); and Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut (M.M.)</aff></contrib-group><author-notes><corresp><bold>Address correspondence to:</bold> Dr. R. R. Gainetdinov, <addr-line>Department of Neuroscience and Brain Technologies, Italian Institute of Technology, Via Morego 30, Genoa, 16163, Italy.</addr-line> E-mail: <email>raul.gainetdinov@iit.it</email></corresp></author-notes><pub-date pub-type="ppub"><month>9</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>9</month><year>2012</year></pub-date><pmc-comment> PMC Release delay is 12 months and 0 days and was based on the
<volume>80</volume><issue>3</issue><fpage>416</fpage><lpage>425</lpage><history><date date-type="received"><day>28</day><month>4</month><year>2011</year></date><date date-type="accepted"><day>10</day><month>6</month><year>2011</year></date></history><permissions><copyright-statement>Copyright © 2011 The American Society for Pharmacology and Experimental Therapeutics</copyright-statement><copyright-year>2011</copyright-year></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zmo00911000416.pdf"></self-uri><abstract><p>The ability of dopamine receptors to interact with other receptor subtypes may provide mechanisms for modulating dopamine-related functions and behaviors. In particular, there is evidence suggesting that the trace amine-associated receptor 1 (TAAR1) affects the dopaminergic system by regulating the firing rate of dopaminergic neurons or by altering dopamine D2 receptor (D2R) responsiveness to ligands. TAAR1 is a Gα<sub>s</sub> protein-coupled receptor that is activated by biogenic amines, “trace amines,” such as β-phenylethylamine (β-PEA) and tyramine that are normally found at low concentrations in the mammalian brain. In the present study, we investigated the biochemical mechanism of interaction between TAAR1 and D2R and the role this interaction plays in D2R-related signaling and behaviors. Using a bioluminescence resonance energy transfer biosensor for cAMP, we demonstrated that the D2R antagonists haloperidol, raclopride, and amisulpride were able to enhance selectively a TAAR1-mediated β-PEA increase of cAMP. Moreover, TAAR1 and D2R were able to form heterodimers when coexpressed in human embryonic kidney 293 cells, and this direct interaction was disrupted in the presence of haloperidol. In addition, in mice lacking TAAR1, haloperidol-induced striatal c-Fos expression and catalepsy were significantly reduced. Taken together, these data suggest that TAAR1 and D2R have functional and physical interactions that could be critical for the modulation of the dopaminergic system by TAAR1 in vivo.</p></abstract><funding-group><award-group><funding-source id="CS100">National Institutes of Health</funding-source><award-id rid="CS100">U01-DA022950</award-id><award-id rid="CS100">P30-DA029925</award-id><award-id rid="CS100">R01-MH073853</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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