Implication of GPER1 in neuroprotection in a mouse model of Parkinson's disease
Abstract This study investigated the contribution of the new G protein-coupled estrogen receptor 1 (GPER1) in neuroprotection by 17β-estradiol in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. In intact mice, administration of GPER1 agonist G1 reprod...
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| Veröffentlicht in: | Neurobiology of aging 2013-03, Vol.34 (3), p.887-901 |
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| creator | Bourque, Mélanie Morissette, Marc Côté, Mélissa Soulet, Denis Di Paolo, Thérèse |
| description | Abstract This study investigated the contribution of the new G protein-coupled estrogen receptor 1 (GPER1) in neuroprotection by 17β-estradiol in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. In intact mice, administration of GPER1 agonist G1 reproduced the effect of 17β-estradiol in increasing striatal dopamine metabolite concentrations as well as the turnover of dopamine. GPER1 antagonist G15 blocked the effect of G1 on homovanillic acid/dopamine ratio and partially for 17β-estradiol. MPTP mice treated with G15 were more susceptible to MPTP toxicity with a greater decrease in striatal dopamine concentration and dopamine transporter specific binding. In MPTP mice, dopamine concentrations as well as dopamine and vesicular monoamine transporter 2 specific binding showed that G1 treatment was as potent as 17β-estradiol in protecting striatum and substantia nigra. G15 antagonized completely the neuroprotective effects of G1 in the striatum and substantia nigra as well as protection by 17β-estradiol in the striatum but partially in the substantia nigra. This study showed an important role of GPER1 in neuroprotection and that G1 is as potent as 17β-estradiol in mediating beneficial effects. |
| doi_str_mv | 10.1016/j.neurobiolaging.2012.05.022 |
| format | Article |
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In intact mice, administration of GPER1 agonist G1 reproduced the effect of 17β-estradiol in increasing striatal dopamine metabolite concentrations as well as the turnover of dopamine. GPER1 antagonist G15 blocked the effect of G1 on homovanillic acid/dopamine ratio and partially for 17β-estradiol. MPTP mice treated with G15 were more susceptible to MPTP toxicity with a greater decrease in striatal dopamine concentration and dopamine transporter specific binding. In MPTP mice, dopamine concentrations as well as dopamine and vesicular monoamine transporter 2 specific binding showed that G1 treatment was as potent as 17β-estradiol in protecting striatum and substantia nigra. G15 antagonized completely the neuroprotective effects of G1 in the striatum and substantia nigra as well as protection by 17β-estradiol in the striatum but partially in the substantia nigra. This study showed an important role of GPER1 in neuroprotection and that G1 is as potent as 17β-estradiol in mediating beneficial effects.</description><identifier>ISSN: 0197-4580</identifier><identifier>EISSN: 1558-1497</identifier><identifier>DOI: 10.1016/j.neurobiolaging.2012.05.022</identifier><identifier>PMID: 22749492</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>17β-estradiol ; Aging ; Animal models ; Animals ; Corpus Striatum - metabolism ; Disease Models, Animal ; Dopamine ; Dopamine - metabolism ; Dopamine Plasma Membrane Transport Proteins - metabolism ; Dopamine transporter ; Estradiol - metabolism ; Estrogen receptors ; GPER1 ; homovanillic acid ; Internal Medicine ; Male ; Metabolites ; Mice ; Mice, Inbred C57BL ; Movement disorders ; MPTP ; Neostriatum ; Nervous system ; Neurodegenerative diseases ; Neurology ; Neuroprotection ; Neurotoxicity ; Parkinson's disease ; Parkinsonian Disorders - metabolism ; Receptors, Estrogen ; Receptors, G-Protein-Coupled - agonists ; Receptors, G-Protein-Coupled - antagonists & inhibitors ; Receptors, G-Protein-Coupled - metabolism ; Striatum ; Substantia nigra ; Substantia Nigra - metabolism ; Vesicular amine transporter ; Vesicular Monoamine Transport Proteins - metabolism</subject><ispartof>Neurobiology of aging, 2013-03, Vol.34 (3), p.887-901</ispartof><rights>Elsevier Inc.</rights><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-9ea92eb85b30886c35aecd8eb5cd2f8560bc458d305305749cb195d5c0c27f0c3</citedby><cites>FETCH-LOGICAL-c540t-9ea92eb85b30886c35aecd8eb5cd2f8560bc458d305305749cb195d5c0c27f0c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neurobiolaging.2012.05.022$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22749492$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bourque, Mélanie</creatorcontrib><creatorcontrib>Morissette, Marc</creatorcontrib><creatorcontrib>Côté, Mélissa</creatorcontrib><creatorcontrib>Soulet, Denis</creatorcontrib><creatorcontrib>Di Paolo, Thérèse</creatorcontrib><title>Implication of GPER1 in neuroprotection in a mouse model of Parkinson's disease</title><title>Neurobiology of aging</title><addtitle>Neurobiol Aging</addtitle><description>Abstract This study investigated the contribution of the new G protein-coupled estrogen receptor 1 (GPER1) in neuroprotection by 17β-estradiol in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. In intact mice, administration of GPER1 agonist G1 reproduced the effect of 17β-estradiol in increasing striatal dopamine metabolite concentrations as well as the turnover of dopamine. GPER1 antagonist G15 blocked the effect of G1 on homovanillic acid/dopamine ratio and partially for 17β-estradiol. MPTP mice treated with G15 were more susceptible to MPTP toxicity with a greater decrease in striatal dopamine concentration and dopamine transporter specific binding. In MPTP mice, dopamine concentrations as well as dopamine and vesicular monoamine transporter 2 specific binding showed that G1 treatment was as potent as 17β-estradiol in protecting striatum and substantia nigra. G15 antagonized completely the neuroprotective effects of G1 in the striatum and substantia nigra as well as protection by 17β-estradiol in the striatum but partially in the substantia nigra. This study showed an important role of GPER1 in neuroprotection and that G1 is as potent as 17β-estradiol in mediating beneficial effects.</description><subject>17β-estradiol</subject><subject>Aging</subject><subject>Animal models</subject><subject>Animals</subject><subject>Corpus Striatum - metabolism</subject><subject>Disease Models, Animal</subject><subject>Dopamine</subject><subject>Dopamine - metabolism</subject><subject>Dopamine Plasma Membrane Transport Proteins - metabolism</subject><subject>Dopamine transporter</subject><subject>Estradiol - metabolism</subject><subject>Estrogen receptors</subject><subject>GPER1</subject><subject>homovanillic acid</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Movement disorders</subject><subject>MPTP</subject><subject>Neostriatum</subject><subject>Nervous system</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neurotoxicity</subject><subject>Parkinson's disease</subject><subject>Parkinsonian Disorders - metabolism</subject><subject>Receptors, Estrogen</subject><subject>Receptors, G-Protein-Coupled - agonists</subject><subject>Receptors, G-Protein-Coupled - antagonists & inhibitors</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Striatum</subject><subject>Substantia nigra</subject><subject>Substantia Nigra - metabolism</subject><subject>Vesicular amine transporter</subject><subject>Vesicular Monoamine Transport Proteins - metabolism</subject><issn>0197-4580</issn><issn>1558-1497</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkm9r1TAUxoMo7jr9CtIXgr5pPUmbJgURxtjmYLDhn9chTU9H7trkmtwK-_ae7k5B3yiEBJLnOefJL2HsDYeKA2_fb6uAS4q9j5O99eG2EsBFBbICIZ6wDZdSl7zp1FO2Ad6pspEajtiLnLcAoBrVPmdHQqimazqxYdeX827yzu59DEUci4ubs8-88KF4aLJLcY_u4Yy2bDHHJSPNA06r-MamOx9yDG9zMfiMNuNL9my0U8ZXj-sx-3Z-9vX0U3l1fXF5enJVOtnAvuzQdgJ7LfsatG5dLS26QWMv3SBGLVvoHQUfapA0KKzreScH6cAJNYKrj9m7Q12K-H3BvDezzw6nyQakkIZLuqxuO87_LRVKqJorDST9cJC6FHNOOJpd8rNN94aDWembrfmTvlnpG5CG6JP99WOnpZ9x-G3-hZsE5wcBEpofHpPJzmNwOPhEnM0Q_f92-vhXITf5QO843eE95m1cUiD8hptMHvNl_QnrR-ACoCZ__RNXpLKs</recordid><startdate>20130301</startdate><enddate>20130301</enddate><creator>Bourque, Mélanie</creator><creator>Morissette, Marc</creator><creator>Côté, Mélissa</creator><creator>Soulet, Denis</creator><creator>Di Paolo, Thérèse</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope></search><sort><creationdate>20130301</creationdate><title>Implication of GPER1 in neuroprotection in a mouse model of Parkinson's disease</title><author>Bourque, Mélanie ; Morissette, Marc ; Côté, Mélissa ; Soulet, Denis ; Di Paolo, Thérèse</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-9ea92eb85b30886c35aecd8eb5cd2f8560bc458d305305749cb195d5c0c27f0c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>17β-estradiol</topic><topic>Aging</topic><topic>Animal models</topic><topic>Animals</topic><topic>Corpus Striatum - metabolism</topic><topic>Disease Models, Animal</topic><topic>Dopamine</topic><topic>Dopamine - metabolism</topic><topic>Dopamine Plasma Membrane Transport Proteins - metabolism</topic><topic>Dopamine transporter</topic><topic>Estradiol - metabolism</topic><topic>Estrogen receptors</topic><topic>GPER1</topic><topic>homovanillic acid</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Metabolites</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Movement disorders</topic><topic>MPTP</topic><topic>Neostriatum</topic><topic>Nervous system</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neurotoxicity</topic><topic>Parkinson's disease</topic><topic>Parkinsonian Disorders - metabolism</topic><topic>Receptors, Estrogen</topic><topic>Receptors, G-Protein-Coupled - agonists</topic><topic>Receptors, G-Protein-Coupled - antagonists & inhibitors</topic><topic>Receptors, G-Protein-Coupled - metabolism</topic><topic>Striatum</topic><topic>Substantia nigra</topic><topic>Substantia Nigra - metabolism</topic><topic>Vesicular amine transporter</topic><topic>Vesicular Monoamine Transport Proteins - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bourque, Mélanie</creatorcontrib><creatorcontrib>Morissette, Marc</creatorcontrib><creatorcontrib>Côté, Mélissa</creatorcontrib><creatorcontrib>Soulet, Denis</creatorcontrib><creatorcontrib>Di Paolo, Thérèse</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Neurobiology of aging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bourque, Mélanie</au><au>Morissette, Marc</au><au>Côté, Mélissa</au><au>Soulet, Denis</au><au>Di Paolo, Thérèse</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Implication of GPER1 in neuroprotection in a mouse model of Parkinson's disease</atitle><jtitle>Neurobiology of aging</jtitle><addtitle>Neurobiol Aging</addtitle><date>2013-03-01</date><risdate>2013</risdate><volume>34</volume><issue>3</issue><spage>887</spage><epage>901</epage><pages>887-901</pages><issn>0197-4580</issn><eissn>1558-1497</eissn><abstract>Abstract This study investigated the contribution of the new G protein-coupled estrogen receptor 1 (GPER1) in neuroprotection by 17β-estradiol in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease. In intact mice, administration of GPER1 agonist G1 reproduced the effect of 17β-estradiol in increasing striatal dopamine metabolite concentrations as well as the turnover of dopamine. GPER1 antagonist G15 blocked the effect of G1 on homovanillic acid/dopamine ratio and partially for 17β-estradiol. MPTP mice treated with G15 were more susceptible to MPTP toxicity with a greater decrease in striatal dopamine concentration and dopamine transporter specific binding. In MPTP mice, dopamine concentrations as well as dopamine and vesicular monoamine transporter 2 specific binding showed that G1 treatment was as potent as 17β-estradiol in protecting striatum and substantia nigra. G15 antagonized completely the neuroprotective effects of G1 in the striatum and substantia nigra as well as protection by 17β-estradiol in the striatum but partially in the substantia nigra. This study showed an important role of GPER1 in neuroprotection and that G1 is as potent as 17β-estradiol in mediating beneficial effects.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>22749492</pmid><doi>10.1016/j.neurobiolaging.2012.05.022</doi><tpages>15</tpages></addata></record> |
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| subjects | 17β-estradiol Aging Animal models Animals Corpus Striatum - metabolism Disease Models, Animal Dopamine Dopamine - metabolism Dopamine Plasma Membrane Transport Proteins - metabolism Dopamine transporter Estradiol - metabolism Estrogen receptors GPER1 homovanillic acid Internal Medicine Male Metabolites Mice Mice, Inbred C57BL Movement disorders MPTP Neostriatum Nervous system Neurodegenerative diseases Neurology Neuroprotection Neurotoxicity Parkinson's disease Parkinsonian Disorders - metabolism Receptors, Estrogen Receptors, G-Protein-Coupled - agonists Receptors, G-Protein-Coupled - antagonists & inhibitors Receptors, G-Protein-Coupled - metabolism Striatum Substantia nigra Substantia Nigra - metabolism Vesicular amine transporter Vesicular Monoamine Transport Proteins - metabolism |
| title | Implication of GPER1 in neuroprotection in a mouse model of Parkinson's disease |
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