Nicotinic receptor stimulation protects nigral dopaminergic neurons in rotenone‐induced Parkinson's disease models
Identifieur interne : 000A14 ( Main/Exploration ); précédent : 000A13; suivant : 000A15Nicotinic receptor stimulation protects nigral dopaminergic neurons in rotenone‐induced Parkinson's disease models
Auteurs : Hiroki Takeuchi [Japon] ; Takashi Yanagida [Japon] ; Masatoshi Inden [Japon] ; Kazuyuki Takata [Japon] ; Yoshihisa Kitamura [Japon] ; Kentaro Yamakawa [Japon] ; Hideyuki Sawada [Japon] ; Yasuhiko Izumi [Japon] ; Noriyuki Yamamoto [Japon] ; Takeshi Kihara [Japon] ; Kengo Uemura [Japon] ; Haruhisa Inoue [Japon] ; Takashi Taniguchi [Japon] ; Akinori Akaike [Japon] ; Ryosuke Takahashi [Japon] ; Shun Shimohama [Japon]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2009-02-01.
English descriptors
Abstract
Parkinson's disease (PD) is the second most common neurodegenerative disease and is characterized by dopaminergic (DA) neuronal cell loss in the substantia nigra. Although the entire pathogenesis of PD is still unclear, both environmental and genetic factors contribute to neurodegeneration. Epidemiologic studies show that prevalence of PD is lower in smokers than in nonsmokers,. Nicotine, a releaser of dopamine from DA neurons, is one of the candidates of antiparkinson agents in tobacco. To assess the protective effect of nicotine against rotenone‐induced DA neuronal cell toxicity, we examined the neuroprotective effects of nicotine in rotenone‐induced PD models in vivo and in vitro. We observed that simultaneous subcutaneous administration of nicotine inhibited both motor deficits and DA neuronal cell loss in the substantia nigra of rotenone‐treated mice. Next, we analyzed the molecular mechanisms of DA neuroprotective effect of nicotine against rotenone‐induced toxicity with primary DA neuronal culture. We found that DA neuroprotective effects of nicotine were inhibited by dihydro‐β‐erythroidine (DHβE), α‐bungarotoxin (αBuTx), and/or PI3K‐Akt/PKB (protein serine/threonine kinase B) inhibitors, demonstrating that rotenone‐toxicity on DA neurons are inhibited via activation of α4β2 or α7 nAChRs‐PI3K‐Akt/PKB pathway or pathways. These results suggest that the rotenone mouse model may be useful for assessing candidate antiparkinson agents, and that nAChR (nicotinic acetylcholine receptor) stimulation can protect DA neurons against degeneration. © 2008 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jnr.21869
Affiliations:
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first="Takashi" last="Taniguchi">Takashi Taniguchi</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurobiology, Kyoto Pharmaceutical University, Kyoto</wicri:regionArea><wicri:noRegion>Kyoto</wicri:noRegion></affiliation></author><author><name sortKey="Akaike, Akinori" sort="Akaike, Akinori" uniqKey="Akaike A" first="Akinori" last="Akaike">Akinori Akaike</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Takahashi, Ryosuke" sort="Takahashi, Ryosuke" uniqKey="Takahashi R" first="Ryosuke" last="Takahashi">Ryosuke Takahashi</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Graduate School of Medicine, Kyoto University, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Shimohama, Shun" sort="Shimohama, Shun" uniqKey="Shimohama S" first="Shun" last="Shimohama">Shun Shimohama</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Sapporo Medical University, Sapporo</wicri:regionArea><wicri:noRegion>Sapporo</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neuroscience Research</title><title level="j" type="abbrev">J. Neurosci. Res.</title><idno type="ISSN">0360-4012</idno><idno type="eISSN">1097-4547</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-02-01">2009-02-01</date><biblScope unit="volume">87</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="576">576</biblScope><biblScope unit="page" to="585">585</biblScope></imprint><idno type="ISSN">0360-4012</idno></series><idno type="istex">5004EBEF263F8C462D17B86531DA5D90AC9C3101</idno><idno type="DOI">10.1002/jnr.21869</idno><idno type="ArticleID">JNR21869</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0360-4012</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>dopaminergic neuron</term><term>neuroprotection</term><term>nicotine</term><term>rotenone</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is the second most common neurodegenerative disease and is characterized by dopaminergic (DA) neuronal cell loss in the substantia nigra. Although the entire pathogenesis of PD is still unclear, both environmental and genetic factors contribute to neurodegeneration. Epidemiologic studies show that prevalence of PD is lower in smokers than in nonsmokers,. Nicotine, a releaser of dopamine from DA neurons, is one of the candidates of antiparkinson agents in tobacco. To assess the protective effect of nicotine against rotenone‐induced DA neuronal cell toxicity, we examined the neuroprotective effects of nicotine in rotenone‐induced PD models in vivo and in vitro. We observed that simultaneous subcutaneous administration of nicotine inhibited both motor deficits and DA neuronal cell loss in the substantia nigra of rotenone‐treated mice. Next, we analyzed the molecular mechanisms of DA neuroprotective effect of nicotine against rotenone‐induced toxicity with primary DA neuronal culture. We found that DA neuroprotective effects of nicotine were inhibited by dihydro‐β‐erythroidine (DHβE), α‐bungarotoxin (αBuTx), and/or PI3K‐Akt/PKB (protein serine/threonine kinase B) inhibitors, demonstrating that rotenone‐toxicity on DA neurons are inhibited via activation of α4β2 or α7 nAChRs‐PI3K‐Akt/PKB pathway or pathways. These results suggest that the rotenone mouse model may be useful for assessing candidate antiparkinson agents, and that nAChR (nicotinic acetylcholine receptor) stimulation can protect DA neurons against degeneration. © 2008 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Japon</li></country><region><li>Région du Kansai</li></region><settlement><li>Kyoto</li></settlement><orgName><li>Université de Kyoto</li></orgName></list><tree><country name="Japon"><region name="Région du Kansai"><name sortKey="Takeuchi, Hiroki" sort="Takeuchi, Hiroki" uniqKey="Takeuchi H" first="Hiroki" last="Takeuchi">Hiroki Takeuchi</name></region><name sortKey="Akaike, Akinori" sort="Akaike, Akinori" uniqKey="Akaike A" first="Akinori" last="Akaike">Akinori Akaike</name><name sortKey="Inden, Masatoshi" sort="Inden, Masatoshi" uniqKey="Inden M" first="Masatoshi" last="Inden">Masatoshi Inden</name><name sortKey="Inoue, Haruhisa" sort="Inoue, Haruhisa" uniqKey="Inoue H" first="Haruhisa" last="Inoue">Haruhisa Inoue</name><name sortKey="Izumi, Yasuhiko" sort="Izumi, Yasuhiko" uniqKey="Izumi Y" first="Yasuhiko" last="Izumi">Yasuhiko Izumi</name><name sortKey="Kihara, Takeshi" sort="Kihara, Takeshi" uniqKey="Kihara T" first="Takeshi" last="Kihara">Takeshi Kihara</name><name sortKey="Kitamura, Yoshihisa" sort="Kitamura, Yoshihisa" uniqKey="Kitamura Y" first="Yoshihisa" last="Kitamura">Yoshihisa Kitamura</name><name sortKey="Sawada, Hideyuki" sort="Sawada, Hideyuki" uniqKey="Sawada H" first="Hideyuki" last="Sawada">Hideyuki Sawada</name><name sortKey="Shimohama, Shun" sort="Shimohama, Shun" uniqKey="Shimohama S" first="Shun" last="Shimohama">Shun Shimohama</name><name sortKey="Takahashi, Ryosuke" sort="Takahashi, Ryosuke" uniqKey="Takahashi R" first="Ryosuke" last="Takahashi">Ryosuke Takahashi</name><name sortKey="Takata, Kazuyuki" sort="Takata, Kazuyuki" uniqKey="Takata K" first="Kazuyuki" last="Takata">Kazuyuki Takata</name><name sortKey="Taniguchi, Takashi" sort="Taniguchi, Takashi" uniqKey="Taniguchi T" first="Takashi" last="Taniguchi">Takashi Taniguchi</name><name sortKey="Uemura, Kengo" sort="Uemura, Kengo" uniqKey="Uemura K" first="Kengo" last="Uemura">Kengo Uemura</name><name sortKey="Yamakawa, Kentaro" sort="Yamakawa, Kentaro" uniqKey="Yamakawa K" first="Kentaro" last="Yamakawa">Kentaro Yamakawa</name><name sortKey="Yamamoto, Noriyuki" sort="Yamamoto, Noriyuki" uniqKey="Yamamoto N" first="Noriyuki" last="Yamamoto">Noriyuki Yamamoto</name><name sortKey="Yanagida, Takashi" sort="Yanagida, Takashi" uniqKey="Yanagida T" first="Takashi" last="Yanagida">Takashi Yanagida</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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