Stimulation of postsynaptic α1b‐ and α2‐adrenergic receptors amplifies dopamine‐mediated locomotor activity in both rats and mice
Identifieur interne : 001C26 ( Istex/Corpus ); précédent : 001C25; suivant : 001C27Stimulation of postsynaptic α1b‐ and α2‐adrenergic receptors amplifies dopamine‐mediated locomotor activity in both rats and mice
Auteurs : Anne-Sophie Villégier ; Candice Drouin ; Jean-Charles Bizot ; Marc Marien ; Jacques Glowinski ; Francis Colpaërt ; Jean-Pol TassinSource :
- Synapse [ 0887-4476 ] ; 2003-12-15.
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Abstract
Recent experiments have shown that mice lacking the α1b‐adrenergic receptor (α1b‐AR KO) are less responsive to the locomotor hyperactivity induced by psychostimulants, such as D‐amphetamine or cocaine, than their wild‐type littermates (WT). These findings suggested that psychostimulants induce locomotor hyperactivity not only because they increase dopamine (DA) transmission, but also because they release norepinephrine (NE). To test whether NE release could increase DA‐mediated locomotor hyperactivity, rats were treated with GBR 12783 (10 mg/kg), a specific inhibitor of the DA transporter, and NE release was enhanced with dexefaroxan (0.63–10 mg/kg), a potent and specific antagonist at α2‐adrenergic receptors. Dexefaroxan increased the GBR 12783‐mediated locomotor response by almost 8‐fold. The role of α1b‐ARs in this effect was then verified in α1b‐AR KO mice: whereas dexefaroxan (1 mg/kg) doubled locomotor hyperactivity induced by GBR 12783 (14 mg/kg) in WT mice, it decreased it by 43% in α1b‐AR KO mice. Finally, to test whether this latter inhibition was related to the occupation of α2‐adrenergic autoreceptors or of α2‐ARs not located on noradrenergic neurons, effects of dexefaroxan on locomotor hyperactivity induced by D‐amphetamine (0.75 mg/kg) were monitored in rats depleted in ascending noradrenergic neurons. In these animals dexefaroxan inhibited by 25–70% D‐amphetamine‐induced locomotor hyperactivity. These data indicate not only that the stimulation of α1b‐ARs increases DA‐mediated locomotor response, but also suggest a significant implication of postsynaptic α2‐ARs. Involvement of these adrenergic receptor mechanisms may be exploited in the therapy of Parkinson's disease. Synapse 50:277–284, 2003. © 2003 Wiley‐Liss, Inc.
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DOI: 10.1002/syn.10267
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mice</title><author><name sortKey="Villegier, Anne Ophie" sort="Villegier, Anne Ophie" uniqKey="Villegier A" first="Anne-Sophie" last="Villégier">Anne-Sophie Villégier</name><affiliation><mods:affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Drouin, Candice" sort="Drouin, Candice" uniqKey="Drouin C" first="Candice" last="Drouin">Candice Drouin</name><affiliation><mods:affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Bizot, Jean Harles" sort="Bizot, Jean Harles" uniqKey="Bizot J" first="Jean-Charles" last="Bizot">Jean-Charles Bizot</name><affiliation><mods:affiliation>Key‐Obs SA, Centre d'innovation, 45074 Orléans, France</mods:affiliation></affiliation></author><author><name sortKey="Marien, Marc" sort="Marien, Marc" uniqKey="Marien M" first="Marc" last="Marien">Marc Marien</name><affiliation><mods:affiliation>Centre de Recherche Pierre Fabre, 81100 Castres, France</mods:affiliation></affiliation></author><author><name sortKey="Glowinski, Jacques" sort="Glowinski, Jacques" uniqKey="Glowinski J" first="Jacques" last="Glowinski">Jacques Glowinski</name><affiliation><mods:affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Colpaert, Francis" sort="Colpaert, Francis" uniqKey="Colpaert F" first="Francis" last="Colpaërt">Francis Colpaërt</name><affiliation><mods:affiliation>Centre de Recherche Pierre Fabre, 81100 Castres, France</mods:affiliation></affiliation></author><author><name sortKey="Tassin, Jean Ol" sort="Tassin, Jean Ol" uniqKey="Tassin J" first="Jean-Pol" last="Tassin">Jean-Pol Tassin</name><affiliation><mods:affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Inserm U. 114, Collège de France, 11, Place Marcelin Berthelot, 75231 Paris Cedex 05, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="ISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2003-12-15">2003-12-15</date><biblScope unit="volume">50</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="277">277</biblScope><biblScope unit="page" to="284">284</biblScope></imprint><idno type="ISSN">0887-4476</idno></series><idno type="istex">2A2CFDAB5313C531CC3DD9B09F6F10205A1560F6</idno><idno type="DOI">10.1002/syn.10267</idno><idno type="ArticleID">SYN10267</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0887-4476</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>6‐OHDA</term><term>D‐amphetamine</term><term>GBR 12783</term><term>NE‐depletion</term><term>dexefaroxan</term><term>α1b‐adrenergic receptor knockout mice</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent experiments have shown that mice lacking the α1b‐adrenergic receptor (α1b‐AR KO) are less responsive to the locomotor hyperactivity induced by psychostimulants, such as D‐amphetamine or cocaine, than their wild‐type littermates (WT). These findings suggested that psychostimulants induce locomotor hyperactivity not only because they increase dopamine (DA) transmission, but also because they release norepinephrine (NE). To test whether NE release could increase DA‐mediated locomotor hyperactivity, rats were treated with GBR 12783 (10 mg/kg), a specific inhibitor of the DA transporter, and NE release was enhanced with dexefaroxan (0.63–10 mg/kg), a potent and specific antagonist at α2‐adrenergic receptors. Dexefaroxan increased the GBR 12783‐mediated locomotor response by almost 8‐fold. The role of α1b‐ARs in this effect was then verified in α1b‐AR KO mice: whereas dexefaroxan (1 mg/kg) doubled locomotor hyperactivity induced by GBR 12783 (14 mg/kg) in WT mice, it decreased it by 43% in α1b‐AR KO mice. Finally, to test whether this latter inhibition was related to the occupation of α2‐adrenergic autoreceptors or of α2‐ARs not located on noradrenergic neurons, effects of dexefaroxan on locomotor hyperactivity induced by D‐amphetamine (0.75 mg/kg) were monitored in rats depleted in ascending noradrenergic neurons. In these animals dexefaroxan inhibited by 25–70% D‐amphetamine‐induced locomotor hyperactivity. These data indicate not only that the stimulation of α1b‐ARs increases DA‐mediated locomotor response, but also suggest a significant implication of postsynaptic α2‐ARs. Involvement of these adrenergic receptor mechanisms may be exploited in the therapy of Parkinson's disease. Synapse 50:277–284, 2003. © 2003 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Anne‐Sophie Villégier</name><affiliations><json:string>Inserm U. 114, Collège de France, 75231 Paris, France</json:string></affiliations></json:item><json:item><name>Candice Drouin</name><affiliations><json:string>Inserm U. 114, Collège de France, 75231 Paris, France</json:string></affiliations></json:item><json:item><name>Jean‐Charles Bizot</name><affiliations><json:string>Key‐Obs SA, Centre d'innovation, 45074 Orléans, France</json:string></affiliations></json:item><json:item><name>Marc Marien</name><affiliations><json:string>Centre de Recherche Pierre Fabre, 81100 Castres, France</json:string></affiliations></json:item><json:item><name>Jacques Glowinski</name><affiliations><json:string>Inserm U. 114, Collège de France, 75231 Paris, France</json:string></affiliations></json:item><json:item><name>Francis Colpaërt</name><affiliations><json:string>Centre de Recherche Pierre Fabre, 81100 Castres, France</json:string></affiliations></json:item><json:item><name>Jean‐Pol Tassin</name><affiliations><json:string>Inserm U. 114, Collège de France, 75231 Paris, France</json:string><json:string>Inserm U. 114, Collège de France, 11, Place Marcelin Berthelot, 75231 Paris Cedex 05, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>GBR 12783</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dexefaroxan</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>α1b‐adrenergic receptor knockout mice</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>6‐OHDA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>NE‐depletion</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>D‐amphetamine</value></json:item></subject><articleId><json:string>SYN10267</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Recent experiments have shown that mice lacking the α1b‐adrenergic receptor (α1b‐AR KO) are less responsive to the locomotor hyperactivity induced by psychostimulants, such as D‐amphetamine or cocaine, than their wild‐type littermates (WT). These findings suggested that psychostimulants induce locomotor hyperactivity not only because they increase dopamine (DA) transmission, but also because they release norepinephrine (NE). To test whether NE release could increase DA‐mediated locomotor hyperactivity, rats were treated with GBR 12783 (10 mg/kg), a specific inhibitor of the DA transporter, and NE release was enhanced with dexefaroxan (0.63–10 mg/kg), a potent and specific antagonist at α2‐adrenergic receptors. Dexefaroxan increased the GBR 12783‐mediated locomotor response by almost 8‐fold. The role of α1b‐ARs in this effect was then verified in α1b‐AR KO mice: whereas dexefaroxan (1 mg/kg) doubled locomotor hyperactivity induced by GBR 12783 (14 mg/kg) in WT mice, it decreased it by 43% in α1b‐AR KO mice. Finally, to test whether this latter inhibition was related to the occupation of α2‐adrenergic autoreceptors or of α2‐ARs not located on noradrenergic neurons, effects of dexefaroxan on locomotor hyperactivity induced by D‐amphetamine (0.75 mg/kg) were monitored in rats depleted in ascending noradrenergic neurons. In these animals dexefaroxan inhibited by 25–70% D‐amphetamine‐induced locomotor hyperactivity. These data indicate not only that the stimulation of α1b‐ARs increases DA‐mediated locomotor response, but also suggest a significant implication of postsynaptic α2‐ARs. Involvement of these adrenergic receptor mechanisms may be exploited in the therapy of Parkinson's disease. Synapse 50:277–284, 2003. © 2003 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>7.928</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1761</abstractCharCount><pdfWordCount>5071</pdfWordCount><pdfCharCount>33238</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>244</abstractWordCount></qualityIndicators><title>Stimulation of postsynaptic α1b‐ and α2‐adrenergic receptors amplifies dopamine‐mediated locomotor activity in both rats and mice</title><refBibs><json:item><author><json:item><name>PH Andersen</name></json:item></author><host><volume>166</volume><pages><last>504</last><first>493</first></pages><author></author><title>Eur J Pharmacol</title></host><title>The dopamine inhibitor GBR 12909: selectivity and molecular mechanism of action</title></json:item><json:item><author><json:item><name>SM Antelman</name></json:item><json:item><name>AR 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medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix></categories><publicationDate>2003</publicationDate><copyrightDate>2003</copyrightDate><doi><json:string>10.1002/syn.10267</json:string></doi><id>2A2CFDAB5313C531CC3DD9B09F6F10205A1560F6</id><score>0.25730258</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/2A2CFDAB5313C531CC3DD9B09F6F10205A1560F6/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/2A2CFDAB5313C531CC3DD9B09F6F10205A1560F6/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/2A2CFDAB5313C531CC3DD9B09F6F10205A1560F6/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Stimulation of postsynaptic α1b‐ and α2‐adrenergic receptors amplifies dopamine‐mediated locomotor activity in both rats and mice</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Copyright © 2003 Wiley‐Liss, Inc.</p></availability><date>2003</date></publicationStmt><notesStmt><note>Fondation Lagrue</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Stimulation of postsynaptic α1b‐ and α2‐adrenergic receptors amplifies dopamine‐mediated locomotor activity in both rats and mice</title><author xml:id="author-1"><persName><forename type="first">Anne‐Sophie</forename><surname>Villégier</surname></persName><affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">Candice</forename><surname>Drouin</surname></persName><affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</affiliation></author><author xml:id="author-3"><persName><forename type="first">Jean‐Charles</forename><surname>Bizot</surname></persName><affiliation>Key‐Obs SA, Centre d'innovation, 45074 Orléans, France</affiliation></author><author xml:id="author-4"><persName><forename type="first">Marc</forename><surname>Marien</surname></persName><affiliation>Centre de Recherche Pierre Fabre, 81100 Castres, France</affiliation></author><author xml:id="author-5"><persName><forename type="first">Jacques</forename><surname>Glowinski</surname></persName><affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</affiliation></author><author xml:id="author-6"><persName><forename type="first">Francis</forename><surname>Colpaërt</surname></persName><affiliation>Centre de Recherche Pierre Fabre, 81100 Castres, France</affiliation></author><author xml:id="author-7"><persName><forename type="first">Jean‐Pol</forename><surname>Tassin</surname></persName><affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</affiliation><affiliation>Inserm U. 114, Collège de France, 11, Place Marcelin Berthelot, 75231 Paris Cedex 05, France</affiliation></author></analytic><monogr><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="pISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><idno type="DOI">10.1002/(ISSN)1098-2396</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2003-12-15"></date><biblScope unit="volume">50</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="277">277</biblScope><biblScope unit="page" to="284">284</biblScope></imprint></monogr><idno type="istex">2A2CFDAB5313C531CC3DD9B09F6F10205A1560F6</idno><idno type="DOI">10.1002/syn.10267</idno><idno type="ArticleID">SYN10267</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2003</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Recent experiments have shown that mice lacking the α1b‐adrenergic receptor (α1b‐AR KO) are less responsive to the locomotor hyperactivity induced by psychostimulants, such as D‐amphetamine or cocaine, than their wild‐type littermates (WT). These findings suggested that psychostimulants induce locomotor hyperactivity not only because they increase dopamine (DA) transmission, but also because they release norepinephrine (NE). To test whether NE release could increase DA‐mediated locomotor hyperactivity, rats were treated with GBR 12783 (10 mg/kg), a specific inhibitor of the DA transporter, and NE release was enhanced with dexefaroxan (0.63–10 mg/kg), a potent and specific antagonist at α2‐adrenergic receptors. Dexefaroxan increased the GBR 12783‐mediated locomotor response by almost 8‐fold. The role of α1b‐ARs in this effect was then verified in α1b‐AR KO mice: whereas dexefaroxan (1 mg/kg) doubled locomotor hyperactivity induced by GBR 12783 (14 mg/kg) in WT mice, it decreased it by 43% in α1b‐AR KO mice. Finally, to test whether this latter inhibition was related to the occupation of α2‐adrenergic autoreceptors or of α2‐ARs not located on noradrenergic neurons, effects of dexefaroxan on locomotor hyperactivity induced by D‐amphetamine (0.75 mg/kg) were monitored in rats depleted in ascending noradrenergic neurons. In these animals dexefaroxan inhibited by 25–70% D‐amphetamine‐induced locomotor hyperactivity. These data indicate not only that the stimulation of α1b‐ARs increases DA‐mediated locomotor response, but also suggest a significant implication of postsynaptic α2‐ARs. Involvement of these adrenergic receptor mechanisms may be exploited in the therapy of Parkinson's disease. Synapse 50:277–284, 2003. © 2003 Wiley‐Liss, Inc.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>GBR 12783</term></item><item><term>dexefaroxan</term></item><item><term>α1b‐adrenergic receptor knockout mice</term></item><item><term>6‐OHDA</term></item><item><term>NE‐depletion</term></item><item><term>D‐amphetamine</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003-03-26">Received</change><change when="2003-07-08">Registration</change><change when="2003-12-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/2A2CFDAB5313C531CC3DD9B09F6F10205A1560F6/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" 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position="20" status="forIssue"><doi origin="wiley" registered="yes">10.1002/syn.10267</doi><idGroup><id type="unit" value="SYN10267"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><copyright ownership="publisher">Copyright © 2003 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptReceived" date="2003-03-26"></event><event type="manuscriptAccepted" date="2003-07-08"></event><event type="firstOnline" date="2003-09-29"></event><event type="publishedOnlineFinalForm" date="2003-09-29"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-04"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-10"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-03"></event></eventGroup><numberingGroup><numbering type="pageFirst">277</numbering><numbering type="pageLast">284</numbering></numberingGroup><correspondenceTo>Inserm U. 114, Collège de France, 11, Place Marcelin Berthelot, 75231 Paris Cedex 05, France</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:SYN.SYN10267.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="55"></count><count type="wordTotal" number="5732"></count></countGroup><titleGroup><title type="main" xml:lang="en">Stimulation of postsynaptic α1b‐ and α2‐adrenergic receptors amplifies dopamine‐mediated locomotor activity in both rats and mice</title><title type="short" xml:lang="en">NE Amplifies DA Locomotor Response</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Anne‐Sophie</givenNames><familyName>Villégier</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Candice</givenNames><familyName>Drouin</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Jean‐Charles</givenNames><familyName>Bizot</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Marc</givenNames><familyName>Marien</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jacques</givenNames><familyName>Glowinski</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Francis</givenNames><familyName>Colpaërt</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Jean‐Pol</givenNames><familyName>Tassin</familyName></personName><contactDetails><email normalForm="jean-pol.tassin@college-de-france.fr">jean‐pol.tassin@college‐de‐france.fr</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FR" type="organization"><unparsedAffiliation>Inserm U. 114, Collège de France, 75231 Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>Key‐Obs SA, Centre d'innovation, 45074 Orléans, France</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Centre de Recherche Pierre Fabre, 81100 Castres, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">GBR 12783</keyword><keyword xml:id="kwd2">dexefaroxan</keyword><keyword xml:id="kwd3">α1b‐adrenergic receptor knockout mice</keyword><keyword xml:id="kwd4">6‐OHDA</keyword><keyword xml:id="kwd5">NE‐depletion</keyword><keyword xml:id="kwd6">D‐amphetamine</keyword></keywordGroup><fundingInfo><fundingAgency>Fondation Lagrue</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Recent experiments have shown that mice lacking the α1b‐adrenergic receptor (α1b‐AR KO) are less responsive to the locomotor hyperactivity induced by psychostimulants, such as D‐amphetamine or cocaine, than their wild‐type littermates (WT). These findings suggested that psychostimulants induce locomotor hyperactivity not only because they increase dopamine (DA) transmission, but also because they release norepinephrine (NE). To test whether NE release could increase DA‐mediated locomotor hyperactivity, rats were treated with GBR 12783 (10 mg/kg), a specific inhibitor of the DA transporter, and NE release was enhanced with dexefaroxan (0.63–10 mg/kg), a potent and specific antagonist at α2‐adrenergic receptors. Dexefaroxan increased the GBR 12783‐mediated locomotor response by almost 8‐fold. The role of α1b‐ARs in this effect was then verified in α1b‐AR KO mice: whereas dexefaroxan (1 mg/kg) doubled locomotor hyperactivity induced by GBR 12783 (14 mg/kg) in WT mice, it decreased it by 43% in α1b‐AR KO mice. Finally, to test whether this latter inhibition was related to the occupation of α2‐adrenergic autoreceptors or of α2‐ARs not located on noradrenergic neurons, effects of dexefaroxan on locomotor hyperactivity induced by D‐amphetamine (0.75 mg/kg) were monitored in rats depleted in ascending noradrenergic neurons. In these animals dexefaroxan inhibited by 25–70% D‐amphetamine‐induced locomotor hyperactivity. These data indicate not only that the stimulation of α1b‐ARs increases DA‐mediated locomotor response, but also suggest a significant implication of postsynaptic α2‐ARs. Involvement of these adrenergic receptor mechanisms may be exploited in the therapy of Parkinson's disease. Synapse 50:277–284, 2003. © 2003 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Stimulation of postsynaptic α1b‐ and α2‐adrenergic receptors amplifies dopamine‐mediated locomotor activity in both rats and mice</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>NE Amplifies DA Locomotor Response</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Stimulation of postsynaptic α1b‐ and α2‐adrenergic receptors amplifies dopamine‐mediated locomotor activity in both rats and mice</title></titleInfo><name type="personal"><namePart type="given">Anne‐Sophie</namePart><namePart type="family">Villégier</namePart><affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Candice</namePart><namePart type="family">Drouin</namePart><affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Charles</namePart><namePart type="family">Bizot</namePart><affiliation>Key‐Obs SA, Centre d'innovation, 45074 Orléans, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marc</namePart><namePart type="family">Marien</namePart><affiliation>Centre de Recherche Pierre Fabre, 81100 Castres, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jacques</namePart><namePart type="family">Glowinski</namePart><affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Francis</namePart><namePart type="family">Colpaërt</namePart><affiliation>Centre de Recherche Pierre Fabre, 81100 Castres, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Pol</namePart><namePart type="family">Tassin</namePart><affiliation>Inserm U. 114, Collège de France, 75231 Paris, France</affiliation><affiliation>Inserm U. 114, Collège de France, 11, Place Marcelin Berthelot, 75231 Paris Cedex 05, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2003-12-15</dateIssued><dateCaptured encoding="w3cdtf">2003-03-26</dateCaptured><dateValid encoding="w3cdtf">2003-07-08</dateValid><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="references">55</extent><extent unit="words">5732</extent></physicalDescription><abstract lang="en">Recent experiments have shown that mice lacking the α1b‐adrenergic receptor (α1b‐AR KO) are less responsive to the locomotor hyperactivity induced by psychostimulants, such as D‐amphetamine or cocaine, than their wild‐type littermates (WT). These findings suggested that psychostimulants induce locomotor hyperactivity not only because they increase dopamine (DA) transmission, but also because they release norepinephrine (NE). To test whether NE release could increase DA‐mediated locomotor hyperactivity, rats were treated with GBR 12783 (10 mg/kg), a specific inhibitor of the DA transporter, and NE release was enhanced with dexefaroxan (0.63–10 mg/kg), a potent and specific antagonist at α2‐adrenergic receptors. Dexefaroxan increased the GBR 12783‐mediated locomotor response by almost 8‐fold. The role of α1b‐ARs in this effect was then verified in α1b‐AR KO mice: whereas dexefaroxan (1 mg/kg) doubled locomotor hyperactivity induced by GBR 12783 (14 mg/kg) in WT mice, it decreased it by 43% in α1b‐AR KO mice. Finally, to test whether this latter inhibition was related to the occupation of α2‐adrenergic autoreceptors or of α2‐ARs not located on noradrenergic neurons, effects of dexefaroxan on locomotor hyperactivity induced by D‐amphetamine (0.75 mg/kg) were monitored in rats depleted in ascending noradrenergic neurons. In these animals dexefaroxan inhibited by 25–70% D‐amphetamine‐induced locomotor hyperactivity. These data indicate not only that the stimulation of α1b‐ARs increases DA‐mediated locomotor response, but also suggest a significant implication of postsynaptic α2‐ARs. Involvement of these adrenergic receptor mechanisms may be exploited in the therapy of Parkinson's disease. Synapse 50:277–284, 2003. © 2003 Wiley‐Liss, Inc.</abstract><note type="funding">Fondation Lagrue</note><subject lang="en"><genre>keywords</genre><topic>GBR 12783</topic><topic>dexefaroxan</topic><topic>α1b‐adrenergic receptor knockout mice</topic><topic>6‐OHDA</topic><topic>NE‐depletion</topic><topic>D‐amphetamine</topic></subject><relatedItem type="host"><titleInfo><title>Synapse</title></titleInfo><titleInfo type="abbreviated"><title>Synapse</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0887-4476</identifier><identifier type="eISSN">1098-2396</identifier><identifier type="DOI">10.1002/(ISSN)1098-2396</identifier><identifier type="PublisherID">SYN</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>50</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>277</start><end>284</end><total>8</total></extent></part></relatedItem><identifier type="istex">2A2CFDAB5313C531CC3DD9B09F6F10205A1560F6</identifier><identifier type="DOI">10.1002/syn.10267</identifier><identifier type="ArticleID">SYN10267</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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