Stereospecific prevention by 17β‐estradiol of MPTP‐induced dopamine depletion in mice
Identifieur interne : 000608 ( Istex/Corpus ); précédent : 000607; suivant : 000609Stereospecific prevention by 17β‐estradiol of MPTP‐induced dopamine depletion in mice
Auteurs : Sophie Callier ; Marc Morissette ; Michelle Grbois ; Thérèse Di PaoloSource :
- Synapse [ 0887-4476 ] ; 2000-09-15.
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Abstract
Neuroprotective activity of estrogens is reported in Alzheimer disease and recently has also been suggested for Parkinson disease, a disease affecting more men than women. To characterize this estrogenic activity, we studied the effects of 17β‐ and 17α‐estradiol treatment (1 μg twice daily 5 days before, during the day of four MPTP (15 mg/kg) injections, and for the following 5 days) on dopamine striatal toxicity induced by the neurotoxin MPTP in retired breeder male C57BL/6 mice. Striatal dopamine concentrations and its metabolites dihydroxyphenylacetic acid and homovanillic acid measured by HPLC in MPTP mice that received 17β‐estradiol were comparable to control animals, whereas MPTP mice treated with saline or 17α‐estradiol showed important decreases of dopamine and its metabolites. Striatal serotonin and its metabolite 5‐hydroxyindoleacetic acid concentrations remained unchanged after MPTP and treatments with steroids. Striatal [3H]GBR 12935 binding autoradiography to the dopamine transporter was as extensively decreased and correlated with dopamine depletion in MPTP mice, whereas this transporter mRNA decrease in the substantia nigra pars compacta was less pronounced. Treatment with steroids did not significantly change [3H]GBR 12935 binding, whereas dopamine transporter mRNA levels were not significantly different from controls. Under the present paradigm in retired breeder male mice, our results show dopaminergic and stereospecificity of estradiol to augment dopamine levels in MPTP‐lesioned mice without protecting against the extensive loss of dopamine terminals and moderate cell body loss. Synapse 37:245–251, 2000. © 2000 Wiley‐Liss, Inc.
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DOI: 10.1002/1098-2396(20000915)37:4<245::AID-SYN1>3.0.CO;2-5
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Striatal [3H]GBR 12935 binding autoradiography to the dopamine transporter was as extensively decreased and correlated with dopamine depletion in MPTP mice, whereas this transporter mRNA decrease in the substantia nigra pars compacta was less pronounced. Treatment with steroids did not significantly change [3H]GBR 12935 binding, whereas dopamine transporter mRNA levels were not significantly different from controls. Under the present paradigm in retired breeder male mice, our results show dopaminergic and stereospecificity of estradiol to augment dopamine levels in MPTP‐lesioned mice without protecting against the extensive loss of dopamine terminals and moderate cell body loss. 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Striatal [3H]GBR 12935 binding autoradiography to the dopamine transporter was as extensively decreased and correlated with dopamine depletion in MPTP mice, whereas this transporter mRNA decrease in the substantia nigra pars compacta was less pronounced. Treatment with steroids did not significantly change [3H]GBR 12935 binding, whereas dopamine transporter mRNA levels were not significantly different from controls. Under the present paradigm in retired breeder male mice, our results show dopaminergic and stereospecificity of estradiol to augment dopamine levels in MPTP‐lesioned mice without protecting against the extensive loss of dopamine terminals and moderate cell body loss. 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Striatal [3H]GBR 12935 binding autoradiography to the dopamine transporter was as extensively decreased and correlated with dopamine depletion in MPTP mice, whereas this transporter mRNA decrease in the substantia nigra pars compacta was less pronounced. Treatment with steroids did not significantly change [3H]GBR 12935 binding, whereas dopamine transporter mRNA levels were not significantly different from controls. Under the present paradigm in retired breeder male mice, our results show dopaminergic and stereospecificity of estradiol to augment dopamine levels in MPTP‐lesioned mice without protecting against the extensive loss of dopamine terminals and moderate cell body loss. 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#af2"><personName><givenNames>Sophie</givenNames><familyName>Callier</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Marc</givenNames><familyName>Morissette</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michelle</givenNames><familyName>Grbois</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Thérèse</givenNames><familyName>Di Paolo</familyName></personName><contactDetails><email>therese.dipaolo@crchul.ulaval.ca</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Centre de Recherches en Endocrinologie Moléculaire, Le Centre Hospitalier Universitaire de Québec, Pavillon CHUL, Québec, Qc, G1V 4G2, and Faculty of Pharmacy, Laval University, Québec, Qc, G1K 7P4, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>INSERM Unit 339, St.‐Antoine Hospital, 75012 Paris, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">17β‐estradiol</keyword><keyword xml:id="kwd2">17α‐estradiol</keyword><keyword xml:id="kwd3">MPTP</keyword><keyword xml:id="kwd4">dopamine</keyword><keyword xml:id="kwd5">dopamine transporter</keyword><keyword xml:id="kwd6">striatum</keyword></keywordGroup><fundingInfo><fundingAgency>MRC of Canada</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Neuroprotective activity of estrogens is reported in Alzheimer disease and recently has also been suggested for Parkinson disease, a disease affecting more men than women. To characterize this estrogenic activity, we studied the effects of 17β‐ and 17α‐estradiol treatment (1 μg twice daily 5 days before, during the day of four MPTP (15 mg/kg) injections, and for the following 5 days) on dopamine striatal toxicity induced by the neurotoxin MPTP in retired breeder male C57BL/6 mice. Striatal dopamine concentrations and its metabolites dihydroxyphenylacetic acid and homovanillic acid measured by HPLC in MPTP mice that received 17β‐estradiol were comparable to control animals, whereas MPTP mice treated with saline or 17α‐estradiol showed important decreases of dopamine and its metabolites. Striatal serotonin and its metabolite 5‐hydroxyindoleacetic acid concentrations remained unchanged after MPTP and treatments with steroids. Striatal [<sup>3</sup>H]GBR 12935 binding autoradiography to the dopamine transporter was as extensively decreased and correlated with dopamine depletion in MPTP mice, whereas this transporter mRNA decrease in the substantia nigra pars compacta was less pronounced. Treatment with steroids did not significantly change [<sup>3</sup>H]GBR 12935 binding, whereas dopamine transporter mRNA levels were not significantly different from controls. Under the present paradigm in retired breeder male mice, our results show dopaminergic and stereospecificity of estradiol to augment dopamine levels in MPTP‐lesioned mice without protecting against the extensive loss of dopamine terminals and moderate cell body loss. Synapse 37:245–251, 2000. © 2000 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Stereospecific prevention by 17β‐estradiol of MPTP‐induced dopamine depletion in mice</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Stereospecific Estradiol Effect in MPTP‐Mice</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Stereospecific prevention by 17β‐estradiol of MPTP‐induced dopamine depletion in mice</title></titleInfo><name type="personal"><namePart type="given">Sophie</namePart><namePart type="family">Callier</namePart><affiliation>Centre de Recherches en Endocrinologie Moléculaire, Le Centre Hospitalier Universitaire de Québec, Pavillon CHUL, Québec, Qc, G1V 4G2, and Faculty of Pharmacy, Laval University, Québec, Qc, G1K 7P4, Canada</affiliation><affiliation>INSERM Unit 339, St.‐Antoine Hospital, 75012 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marc</namePart><namePart type="family">Morissette</namePart><affiliation>Centre de Recherches en Endocrinologie Moléculaire, Le Centre Hospitalier Universitaire de Québec, Pavillon CHUL, Québec, Qc, G1V 4G2, and Faculty of Pharmacy, Laval University, Québec, Qc, G1K 7P4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michelle</namePart><namePart type="family">Grbois</namePart><affiliation>Centre de Recherches en Endocrinologie Moléculaire, Le Centre Hospitalier Universitaire de Québec, Pavillon CHUL, Québec, Qc, G1V 4G2, and Faculty of Pharmacy, Laval University, Québec, Qc, G1K 7P4, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thérèse</namePart><namePart type="family">Di Paolo</namePart><affiliation>Centre de Recherches en Endocrinologie Moléculaire, Le Centre Hospitalier Universitaire de Québec, Pavillon CHUL, Québec, Qc, G1V 4G2, and Faculty of Pharmacy, Laval University, Québec, Qc, G1K 7P4, Canada</affiliation><affiliation>Centre de Recherches en Endocrinologie Moléculaire, Le Centre Hospitalier Universitaire de Québec, Pavillon CHUL, 2705, Boulevard Laurier, Québec, Qc, Canada, G1V 4G2</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>John Wiley & Sons, Inc.</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2000-09-15</dateIssued><dateCaptured encoding="w3cdtf">1999-08-17</dateCaptured><dateValid encoding="w3cdtf">1999-11-08</dateValid><copyrightDate encoding="w3cdtf">2000</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">2</extent><extent unit="references">52</extent><extent unit="words">4945</extent></physicalDescription><abstract lang="en">Neuroprotective activity of estrogens is reported in Alzheimer disease and recently has also been suggested for Parkinson disease, a disease affecting more men than women. To characterize this estrogenic activity, we studied the effects of 17β‐ and 17α‐estradiol treatment (1 μg twice daily 5 days before, during the day of four MPTP (15 mg/kg) injections, and for the following 5 days) on dopamine striatal toxicity induced by the neurotoxin MPTP in retired breeder male C57BL/6 mice. Striatal dopamine concentrations and its metabolites dihydroxyphenylacetic acid and homovanillic acid measured by HPLC in MPTP mice that received 17β‐estradiol were comparable to control animals, whereas MPTP mice treated with saline or 17α‐estradiol showed important decreases of dopamine and its metabolites. Striatal serotonin and its metabolite 5‐hydroxyindoleacetic acid concentrations remained unchanged after MPTP and treatments with steroids. Striatal [3H]GBR 12935 binding autoradiography to the dopamine transporter was as extensively decreased and correlated with dopamine depletion in MPTP mice, whereas this transporter mRNA decrease in the substantia nigra pars compacta was less pronounced. Treatment with steroids did not significantly change [3H]GBR 12935 binding, whereas dopamine transporter mRNA levels were not significantly different from controls. Under the present paradigm in retired breeder male mice, our results show dopaminergic and stereospecificity of estradiol to augment dopamine levels in MPTP‐lesioned mice without protecting against the extensive loss of dopamine terminals and moderate cell body loss. Synapse 37:245–251, 2000. © 2000 Wiley‐Liss, Inc.</abstract><note type="funding">MRC of Canada</note><subject lang="en"><genre>keywords</genre><topic>17β‐estradiol</topic><topic>17α‐estradiol</topic><topic>MPTP</topic><topic>dopamine</topic><topic>dopamine transporter</topic><topic>striatum</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>2000</date><detail type="volume"><caption>vol.</caption><number>37</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>245</start><end>251</end><total>7</total></extent></part></relatedItem><identifier type="istex">4D2CD72C7E2B927E2AF68157BB11DCFC5A9F3D2C</identifier><identifier type="DOI">10.1002/1098-2396(20000915)37:4<245::AID-SYN1>3.0.CO;2-5</identifier><identifier type="ArticleID">SYN1</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2000 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>John Wiley & Sons, Inc.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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