Dopamine D3 receptor‐preferring agonists induce neurotrophic effects on mesencephalic dopamine neurons
Identifieur interne : 001806 ( Main/Corpus ); précédent : 001805; suivant : 001807Dopamine D3 receptor‐preferring agonists induce neurotrophic effects on mesencephalic dopamine neurons
Auteurs : Fang Du ; Rui Li ; Yuangui Huang ; Xuping Li ; Weidong LeSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2005-11.
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Abstract
Anti‐parkinsonian agents, pramipexole (PPX) and ropinirole (ROP), have been reported to possess neuroprotective properties, both in vitro and in vivo. The mechanisms underlying neuroprotection afforded by the D3‐preferring receptor agonists remain poorly understood. The present study demonstrates that incubation of primary mesencephalic cultures with PPX and ROP or the conditioned medium from PPX‐ or ROP‐treated primary cultures induced a marked increase in the number of dopamine (DA) neurons in the cultures. Similar effects can be observed after incubating with the conditioned medium derived from PPX‐ and ROP‐treated substantia nigra astroglia. Meanwhile, PPX and ROP can protect the primary cells from insult of 1‐methyl‐4‐phenylpyridinium (MPP+), the active metabolite of the neurotoxin 1‐methyl‐4‐phenyl‐1,2,5,6‐tetrahydropyridine (MPTP). Furthermore, the neurotrophic effects of PPX and ROP on mesencephalic dopamine neurons could be significantly blocked by D3 receptor antagonist, but not by D2 receptor antagonist. Moreover, we found that the levels of glial cell line‐derived neurotrophic factor (GDNF) and brain‐derived neurotrophic factor (BDNF) in the conditioned medium of mesencephalic cultures treated with PPX and ROP were significantly increased. Blocking GDNF and BDNF with the neutralizing antibodies, the neurotrophic effects of PPX and ROP were greatly diminished. These results suggest that D3 dopamine receptor‐preferring agonists, PPX and ROP, exert neurotrophic effects on cultured DA neurons by modulating the production of endogenous GDNF and BDNF, which may participate in their neuroprotection.
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DOI: 10.1111/j.1460-9568.2005.04438.x
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China</mods:affiliation></affiliation></author><author><name sortKey="Li, Rui" sort="Li, Rui" uniqKey="Li R" first="Rui" last="Li">Rui Li</name><affiliation><mods:affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Shaanxi Provincial People's Hospital, Xi'an, 710068, P.R. China</mods:affiliation></affiliation></author><author><name sortKey="Huang, Yuangui" sort="Huang, Yuangui" uniqKey="Huang Y" first="Yuangui" last="Huang">Yuangui Huang</name><affiliation><mods:affiliation>Neurology Department of Xijing Hospital, 17 Changle Western Road, Xi'an, 710032, P.R. China</mods:affiliation></affiliation></author><author><name sortKey="Li, Xuping" sort="Li, Xuping" uniqKey="Li X" first="Xuping" last="Li">Xuping Li</name><affiliation><mods:affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</mods:affiliation></affiliation></author><author><name sortKey="Le, Weidong" sort="Le, Weidong" uniqKey="Le W" first="Weidong" last="Le">Weidong Le</name><affiliation><mods:affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. 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China</mods:affiliation></affiliation></author><author><name sortKey="Huang, Yuangui" sort="Huang, Yuangui" uniqKey="Huang Y" first="Yuangui" last="Huang">Yuangui Huang</name><affiliation><mods:affiliation>Neurology Department of Xijing Hospital, 17 Changle Western Road, Xi'an, 710032, P.R. China</mods:affiliation></affiliation></author><author><name sortKey="Li, Xuping" sort="Li, Xuping" uniqKey="Li X" first="Xuping" last="Li">Xuping Li</name><affiliation><mods:affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</mods:affiliation></affiliation></author><author><name sortKey="Le, Weidong" sort="Le, Weidong" uniqKey="Le W" first="Weidong" last="Le">Weidong Le</name><affiliation><mods:affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neuroscience</title><idno type="ISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><imprint><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-11">2005-11</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="2422">2422</biblScope><biblScope unit="page" to="2430">2430</biblScope></imprint><idno type="ISSN">0953-816X</idno></series><idno type="istex">61FED2623A7F6B8FE558DFAD9B45009D7530944F</idno><idno type="DOI">10.1111/j.1460-9568.2005.04438.x</idno><idno type="ArticleID">EJN4438</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>brain‐derived neurotrophic factor</term><term>glial cell line‐derived neurotrophic factor</term><term>pramipexole</term><term>ropinirole</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Anti‐parkinsonian agents, pramipexole (PPX) and ropinirole (ROP), have been reported to possess neuroprotective properties, both in vitro and in vivo. The mechanisms underlying neuroprotection afforded by the D3‐preferring receptor agonists remain poorly understood. The present study demonstrates that incubation of primary mesencephalic cultures with PPX and ROP or the conditioned medium from PPX‐ or ROP‐treated primary cultures induced a marked increase in the number of dopamine (DA) neurons in the cultures. Similar effects can be observed after incubating with the conditioned medium derived from PPX‐ and ROP‐treated substantia nigra astroglia. Meanwhile, PPX and ROP can protect the primary cells from insult of 1‐methyl‐4‐phenylpyridinium (MPP+), the active metabolite of the neurotoxin 1‐methyl‐4‐phenyl‐1,2,5,6‐tetrahydropyridine (MPTP). Furthermore, the neurotrophic effects of PPX and ROP on mesencephalic dopamine neurons could be significantly blocked by D3 receptor antagonist, but not by D2 receptor antagonist. Moreover, we found that the levels of glial cell line‐derived neurotrophic factor (GDNF) and brain‐derived neurotrophic factor (BDNF) in the conditioned medium of mesencephalic cultures treated with PPX and ROP were significantly increased. Blocking GDNF and BDNF with the neutralizing antibodies, the neurotrophic effects of PPX and ROP were greatly diminished. These results suggest that D3 dopamine receptor‐preferring agonists, PPX and ROP, exert neurotrophic effects on cultured DA neurons by modulating the production of endogenous GDNF and BDNF, which may participate in their neuroprotection.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Fang Du</name><affiliations><json:string>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</json:string><json:string>Neurology Department of Xijing Hospital, 17 Changle Western Road, Xi'an, 710032, P.R. China</json:string></affiliations></json:item><json:item><name>Rui Li</name><affiliations><json:string>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</json:string><json:string>Department of Neurology, Shaanxi Provincial People's Hospital, Xi'an, 710068, P.R. China</json:string></affiliations></json:item><json:item><name>Yuangui Huang</name><affiliations><json:string>Neurology Department of Xijing Hospital, 17 Changle Western Road, Xi'an, 710032, P.R. China</json:string></affiliations></json:item><json:item><name>Xuping Li</name><affiliations><json:string>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</json:string></affiliations></json:item><json:item><name>Weidong Le</name><affiliations><json:string>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>brain‐derived neurotrophic factor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glial cell line‐derived neurotrophic factor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pramipexole</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ropinirole</value></json:item></subject><articleId><json:string>EJN4438</json:string></articleId><language><json:string>eng</json:string></language><abstract>Anti‐parkinsonian agents, pramipexole (PPX) and ropinirole (ROP), have been reported to possess neuroprotective properties, both in vitro and in vivo. The mechanisms underlying neuroprotection afforded by the D3‐preferring receptor agonists remain poorly understood. The present study demonstrates that incubation of primary mesencephalic cultures with PPX and ROP or the conditioned medium from PPX‐ or ROP‐treated primary cultures induced a marked increase in the number of dopamine (DA) neurons in the cultures. Similar effects can be observed after incubating with the conditioned medium derived from PPX‐ and ROP‐treated substantia nigra astroglia. Meanwhile, PPX and ROP can protect the primary cells from insult of 1‐methyl‐4‐phenylpyridinium (MPP+), the active metabolite of the neurotoxin 1‐methyl‐4‐phenyl‐1,2,5,6‐tetrahydropyridine (MPTP). Furthermore, the neurotrophic effects of PPX and ROP on mesencephalic dopamine neurons could be significantly blocked by D3 receptor antagonist, but not by D2 receptor antagonist. Moreover, we found that the levels of glial cell line‐derived neurotrophic factor (GDNF) and brain‐derived neurotrophic factor (BDNF) in the conditioned medium of mesencephalic cultures treated with PPX and ROP were significantly increased. Blocking GDNF and BDNF with the neutralizing antibodies, the neurotrophic effects of PPX and ROP were greatly diminished. These results suggest that D3 dopamine receptor‐preferring agonists, PPX and ROP, exert neurotrophic effects on cultured DA neurons by modulating the production of endogenous GDNF and BDNF, which may participate in their neuroprotection.</abstract><qualityIndicators><score>8.164</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1631</abstractCharCount><pdfWordCount>6479</pdfWordCount><pdfCharCount>39525</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>222</abstractWordCount></qualityIndicators><title>Dopamine D3 receptor‐preferring agonists induce neurotrophic effects on mesencephalic dopamine neurons</title><genre><json:string>article</json:string></genre><host><volume>22</volume><publisherId><json:string>EJN</json:string></publisherId><pages><total>9</total><last>2430</last><first>2422</first></pages><issn><json:string>0953-816X</json:string></issn><issue>10</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-9568</json:string></eissn><title>European Journal of Neuroscience</title><doi><json:string>10.1111/(ISSN)1460-9568</json:string></doi></host><publicationDate>2005</publicationDate><copyrightDate>2005</copyrightDate><doi><json:string>10.1111/j.1460-9568.2005.04438.x</json:string></doi><id>61FED2623A7F6B8FE558DFAD9B45009D7530944F</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/61FED2623A7F6B8FE558DFAD9B45009D7530944F/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/61FED2623A7F6B8FE558DFAD9B45009D7530944F/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/61FED2623A7F6B8FE558DFAD9B45009D7530944F/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Dopamine D3 receptor‐preferring agonists induce neurotrophic effects on mesencephalic dopamine neurons</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2005</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Dopamine D3 receptor‐preferring agonists induce neurotrophic effects on mesencephalic dopamine neurons</title><author><persName><forename type="first">Fang</forename><surname>Du</surname></persName><note type="biography">F.D. and R.L. contributed equally to this work.</note><affiliation>F.D. and R.L. contributed equally to this work.</affiliation><affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</affiliation><affiliation>Neurology Department of Xijing Hospital, 17 Changle Western Road, Xi'an, 710032, P.R. China</affiliation></author><author><persName><forename type="first">Rui</forename><surname>Li</surname></persName><note type="biography">F.D. and R.L. contributed equally to this work.</note><affiliation>F.D. and R.L. contributed equally to this work.</affiliation><affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</affiliation><affiliation>Department of Neurology, Shaanxi Provincial People's Hospital, Xi'an, 710068, P.R. China</affiliation></author><author><persName><forename type="first">Yuangui</forename><surname>Huang</surname></persName><affiliation>Neurology Department of Xijing Hospital, 17 Changle Western Road, Xi'an, 710032, P.R. China</affiliation></author><author><persName><forename type="first">Xuping</forename><surname>Li</surname></persName><affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</affiliation></author><author><persName><forename type="first">Weidong</forename><surname>Le</surname></persName><affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</affiliation></author></analytic><monogr><title level="j">European Journal of Neuroscience</title><idno type="pISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><idno type="DOI">10.1111/(ISSN)1460-9568</idno><imprint><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-11"></date><biblScope unit="volume">22</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="2422">2422</biblScope><biblScope unit="page" to="2430">2430</biblScope></imprint></monogr><idno type="istex">61FED2623A7F6B8FE558DFAD9B45009D7530944F</idno><idno type="DOI">10.1111/j.1460-9568.2005.04438.x</idno><idno type="ArticleID">EJN4438</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Anti‐parkinsonian agents, pramipexole (PPX) and ropinirole (ROP), have been reported to possess neuroprotective properties, both in vitro and in vivo. The mechanisms underlying neuroprotection afforded by the D3‐preferring receptor agonists remain poorly understood. The present study demonstrates that incubation of primary mesencephalic cultures with PPX and ROP or the conditioned medium from PPX‐ or ROP‐treated primary cultures induced a marked increase in the number of dopamine (DA) neurons in the cultures. Similar effects can be observed after incubating with the conditioned medium derived from PPX‐ and ROP‐treated substantia nigra astroglia. Meanwhile, PPX and ROP can protect the primary cells from insult of 1‐methyl‐4‐phenylpyridinium (MPP+), the active metabolite of the neurotoxin 1‐methyl‐4‐phenyl‐1,2,5,6‐tetrahydropyridine (MPTP). Furthermore, the neurotrophic effects of PPX and ROP on mesencephalic dopamine neurons could be significantly blocked by D3 receptor antagonist, but not by D2 receptor antagonist. Moreover, we found that the levels of glial cell line‐derived neurotrophic factor (GDNF) and brain‐derived neurotrophic factor (BDNF) in the conditioned medium of mesencephalic cultures treated with PPX and ROP were significantly increased. Blocking GDNF and BDNF with the neutralizing antibodies, the neurotrophic effects of PPX and ROP were greatly diminished. These results suggest that D3 dopamine receptor‐preferring agonists, PPX and ROP, exert neurotrophic effects on cultured DA neurons by modulating the production of endogenous GDNF and BDNF, which may participate in their neuroprotection.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>brain‐derived neurotrophic factor</term></item><item><term>glial cell line‐derived neurotrophic factor</term></item><item><term>pramipexole</term></item><item><term>ropinirole</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/61FED2623A7F6B8FE558DFAD9B45009D7530944F/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Science Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1460-9568</doi><issn type="print">0953-816X</issn><issn type="electronic">1460-9568</issn><idGroup><id type="product" value="EJN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROSCIENCE">European Journal of Neuroscience</title></titleGroup></publicationMeta><publicationMeta level="part" position="11010"><doi origin="wiley">10.1111/ejn.2005.22.issue-10</doi><numberingGroup><numbering type="journalVolume" number="22">22</numbering><numbering type="journalIssue" number="10">10</numbering></numberingGroup><coverDate startDate="2005-11">November 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="4" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2005.04438.x</doi><idGroup><id type="unit" value="EJN4438"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2005-11-23"></event><event type="publishedOnlineFinalForm" date="2005-11-23"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-02"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="2422">2422</numbering><numbering type="pageLast" number="2430">2430</numbering></numberingGroup><correspondenceTo>Dr W. Le, Department of Neurology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
E‐mail: <email>weidongl@bcm.tmc.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN4438.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 22 December 2004, revised 4 June 2005, 24 July 2005 and 27 August 2005, accepted 31 August 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="10"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="36"></count><count type="wordTotal" number="7037"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Dopamine D3 receptor‐preferring agonists induce neurotrophic effects on mesencephalic dopamine neurons</title><title type="shortAuthors">F. Du <i>et al</i>.</title><title type="short">Dopamine agonists and neurotrophic effects</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2" noteRef="#fn1"><personName><givenNames>Fang</givenNames><familyName>Du</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a3" noteRef="#fn1"><personName><givenNames>Rui</givenNames><familyName>Li</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>Yuangui</givenNames><familyName>Huang</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Xuping</givenNames><familyName>Li</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Weidong</givenNames><familyName>Le</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="CN"><unparsedAffiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="CN"><unparsedAffiliation>Neurology Department of Xijing Hospital, 17 Changle Western Road, Xi'an, 710032, P.R. China</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="CN"><unparsedAffiliation>Department of Neurology, Shaanxi Provincial People's Hospital, Xi'an, 710068, P.R. China</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">brain‐derived neurotrophic factor</keyword><keyword xml:id="k2">glial cell line‐derived neurotrophic factor</keyword><keyword xml:id="k3">pramipexole</keyword><keyword xml:id="k4">ropinirole</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Anti‐parkinsonian agents, pramipexole (PPX) and ropinirole (ROP), have been reported to possess neuroprotective properties, both <i>in vitro</i> and <i>in vivo</i>. The mechanisms underlying neuroprotection afforded by the D3‐preferring receptor agonists remain poorly understood. The present study demonstrates that incubation of primary mesencephalic cultures with PPX and ROP or the conditioned medium from PPX‐ or ROP‐treated primary cultures induced a marked increase in the number of dopamine (DA) neurons in the cultures. Similar effects can be observed after incubating with the conditioned medium derived from PPX‐ and ROP‐treated substantia nigra astroglia. Meanwhile, PPX and ROP can protect the primary cells from insult of 1‐methyl‐4‐phenylpyridinium (MPP<sup>+</sup>), the active metabolite of the neurotoxin 1‐methyl‐4‐phenyl‐1,2,5,6‐tetrahydropyridine (MPTP). Furthermore, the neurotrophic effects of PPX and ROP on mesencephalic dopamine neurons could be significantly blocked by D3 receptor antagonist, but not by D2 receptor antagonist. Moreover, we found that the levels of glial cell line‐derived neurotrophic factor (GDNF) and brain‐derived neurotrophic factor (BDNF) in the conditioned medium of mesencephalic cultures treated with PPX and ROP were significantly increased. Blocking GDNF and BDNF with the neutralizing antibodies, the neurotrophic effects of PPX and ROP were greatly diminished. These results suggest that D3 dopamine receptor‐preferring agonists, PPX and ROP, exert neurotrophic effects on cultured DA neurons by modulating the production of endogenous GDNF and BDNF, which may participate in their neuroprotection.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><label>*</label><p> F.D. and R.L. contributed equally to this work.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Dopamine D3 receptor‐preferring agonists induce neurotrophic effects on mesencephalic dopamine neurons</title></titleInfo><titleInfo type="abbreviated"><title>Dopamine agonists and neurotrophic effects</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Dopamine D3 receptor‐preferring agonists induce neurotrophic effects on mesencephalic dopamine neurons</title></titleInfo><name type="personal"><namePart type="given">Fang</namePart><namePart type="family">Du</namePart><affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</affiliation><affiliation>Neurology Department of Xijing Hospital, 17 Changle Western Road, Xi'an, 710032, P.R. China</affiliation><description>F.D. and R.L. contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rui</namePart><namePart type="family">Li</namePart><affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</affiliation><affiliation>Department of Neurology, Shaanxi Provincial People's Hospital, Xi'an, 710068, P.R. China</affiliation><description>F.D. and R.L. contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yuangui</namePart><namePart type="family">Huang</namePart><affiliation>Neurology Department of Xijing Hospital, 17 Changle Western Road, Xi'an, 710032, P.R. China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Xuping</namePart><namePart type="family">Li</namePart><affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Weidong</namePart><namePart type="family">Le</namePart><affiliation>Joint Laboratory of Institutes of Biomedical Sciences, Ruijin Hospital, Jiao Tong University Medical School, and Institute of Health Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200025, P. R. China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Science Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2005-11</dateIssued><edition>Received 22 December 2004, revised 4 June 2005, 24 July 2005 and 27 August 2005, accepted 31 August 2005</edition><copyrightDate encoding="w3cdtf">2005</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">10</extent><extent unit="references">36</extent><extent unit="words">7037</extent></physicalDescription><abstract lang="en">Anti‐parkinsonian agents, pramipexole (PPX) and ropinirole (ROP), have been reported to possess neuroprotective properties, both in vitro and in vivo. The mechanisms underlying neuroprotection afforded by the D3‐preferring receptor agonists remain poorly understood. The present study demonstrates that incubation of primary mesencephalic cultures with PPX and ROP or the conditioned medium from PPX‐ or ROP‐treated primary cultures induced a marked increase in the number of dopamine (DA) neurons in the cultures. Similar effects can be observed after incubating with the conditioned medium derived from PPX‐ and ROP‐treated substantia nigra astroglia. Meanwhile, PPX and ROP can protect the primary cells from insult of 1‐methyl‐4‐phenylpyridinium (MPP+), the active metabolite of the neurotoxin 1‐methyl‐4‐phenyl‐1,2,5,6‐tetrahydropyridine (MPTP). Furthermore, the neurotrophic effects of PPX and ROP on mesencephalic dopamine neurons could be significantly blocked by D3 receptor antagonist, but not by D2 receptor antagonist. Moreover, we found that the levels of glial cell line‐derived neurotrophic factor (GDNF) and brain‐derived neurotrophic factor (BDNF) in the conditioned medium of mesencephalic cultures treated with PPX and ROP were significantly increased. Blocking GDNF and BDNF with the neutralizing antibodies, the neurotrophic effects of PPX and ROP were greatly diminished. These results suggest that D3 dopamine receptor‐preferring agonists, PPX and ROP, exert neurotrophic effects on cultured DA neurons by modulating the production of endogenous GDNF and BDNF, which may participate in their neuroprotection.</abstract><subject lang="en"><genre>Keywords</genre><topic>brain‐derived neurotrophic factor</topic><topic>glial cell line‐derived neurotrophic factor</topic><topic>pramipexole</topic><topic>ropinirole</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>2422</start><end>2430</end><total>9</total></extent></part></relatedItem><identifier type="istex">61FED2623A7F6B8FE558DFAD9B45009D7530944F</identifier><identifier type="DOI">10.1111/j.1460-9568.2005.04438.x</identifier><identifier type="ArticleID">EJN4438</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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