ParkinsonFranceV1, Hal, Checkpoint, bibRecord, 000276

Tyrosine hydroxylase expression and activity in nigrostriatal dopaminergic neurons of MPTP-treated mice at the presymptomatic and symptomatic stages of parkinsonism

Identifieur interne : 000276 ( Hal/Checkpoint ); précédent : 000275; suivant : 000277

Tyrosine hydroxylase expression and activity in nigrostriatal dopaminergic neurons of MPTP-treated mice at the presymptomatic and symptomatic stages of parkinsonism

Auteurs : E. A. Kozina ; Gr Khakimova ; V. G. Khaindrava [France] ; V. G. Kucheryanu ; N. E. Vorobyeva ; A. N. Krasnov ; S. G. Georgieva ; L. Kerkerian-Legoff [France] ; M. V. Ugrumov

Source :

Journal of the Neurological Sciences [ 0022-510X ] ; 2014-05.

RBID : Hal:hal-01112598

Abstract

Progressive degeneration of nigrostriatal dopaminergic (DA-ergic) neurons is a key component in the pathogenesis of Parkinson's disease, which develops for a long time at the preclinical stage with no motor dysfunctions due to the initiation of compensatory processes. The goal of this study was to evaluate the changes in surviving nigrostriatal DA-ergic neurons with focus on tyrosine hydroxylase (TH) in MPTP-treated mice at the presymptomatic and early symptomatic stages of parkinsonism. According to our data, a partial degeneration of DA-ergic neurons at the presymptomatic stage was accompanied by: (i) no change in TH mRNA content in the substantia nigra (SN) suggesting a compensatory increase of TH gene expression in individual neurons; (ii) a decrease of TH protein content in the nigrostriatal system and no change in individual neurons, suggesting a slowdown of TH translation. When comparing DA-ergic neurons at the early symptomatic stage and presymptomatic stage, it becomes evident: (i) a decrease of TH mRNA content in the SN and hence gene expression in individual neurons; (ii) a decrease of TH content in the striatum and its increase in the SN and individual neurons suggesting an acceleration of TH translation. TH activity, an index of the rate of DA synthesis, was unchanged in the SN and decreased in the striatum to the same degree at both stages of parkinsonism. In the meantime, TH activity in individual neurons appeared to be compensatory increased, but to a higher degree at the symptomatic stage than at the presymptomatic one. These data first show that DA depletion, which provokes motor dysfunction, is not a result of the decrease of TH activity and the rate of DA synthesis but is rather related to either a decrease of DA release or an increase of DA uptake in striatal DA-ergic axons.Copyright © 2014 Elsevier B.V. All rights reserved.

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https://hal.archives-ouvertes.fr/hal-01112598

DOI: 10.1016/j.jns.2014.03.028

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<front><div type="abstract" xml:lang="en">Progressive degeneration of nigrostriatal dopaminergic (DA-ergic) neurons is a key component in the pathogenesis of Parkinson's disease, which develops for a long time at the preclinical stage with no motor dysfunctions due to the initiation of compensatory processes. The goal of this study was to evaluate the changes in surviving nigrostriatal DA-ergic neurons with focus on tyrosine hydroxylase (TH) in MPTP-treated mice at the presymptomatic and early symptomatic stages of parkinsonism. According to our data, a partial degeneration of DA-ergic neurons at the presymptomatic stage was accompanied by: (i) no change in TH mRNA content in the substantia nigra (SN) suggesting a compensatory increase of TH gene expression in individual neurons; (ii) a decrease of TH protein content in the nigrostriatal system and no change in individual neurons, suggesting a slowdown of TH translation. When comparing DA-ergic neurons at the early symptomatic stage and presymptomatic stage, it becomes evident: (i) a decrease of TH mRNA content in the SN and hence gene expression in individual neurons; (ii) a decrease of TH content in the striatum and its increase in the SN and individual neurons suggesting an acceleration of TH translation. TH activity, an index of the rate of DA synthesis, was unchanged in the SN and decreased in the striatum to the same degree at both stages of parkinsonism. In the meantime, TH activity in individual neurons appeared to be compensatory increased, but to a higher degree at the symptomatic stage than at the presymptomatic one. These data first show that DA depletion, which provokes motor dysfunction, is not a result of the decrease of TH activity and the rate of DA synthesis but is rather related to either a decrease of DA release or an increase of DA uptake in striatal DA-ergic axons.Copyright © 2014 Elsevier B.V. All rights reserved.</div>
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            <author role="aut">              <persName>                <forename type="first">V.G.</forename>
                <surname>Khaindrava</surname>
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              <idno type="halauthorid">1124363</idno>
              <affiliation ref="#struct-199397"></affiliation>
            </author>
            <author role="aut">              <persName>                <forename type="first">V.G.</forename>
                <surname>Kucheryanu</surname>
              </persName>
              <idno type="halauthorid">1124364</idno>
            </author>
            <author role="aut">              <persName>                <forename type="first">N.E.</forename>
                <surname>Vorobyeva</surname>
              </persName>
              <idno type="halauthorid">1124365</idno>
            </author>
            <author role="aut">              <persName>                <forename type="first">A.N.</forename>
                <surname>Krasnov</surname>
              </persName>
              <idno type="halauthorid">273681</idno>
            </author>
            <author role="aut">              <persName>                <forename type="first">S.G.</forename>
                <surname>Georgieva</surname>
              </persName>
              <idno type="halauthorid">1124366</idno>
            </author>
            <author role="aut">              <persName>                <forename type="first">L.</forename>
                <surname>Kerkerian-Legoff</surname>
              </persName>
              <idno type="halauthorid">869023</idno>
              <affiliation ref="#struct-199397"></affiliation>
            </author>
            <author role="aut">              <persName>                <forename type="first">M.V.</forename>
                <surname>Ugrumov</surname>
              </persName>
              <idno type="halauthorid">141052</idno>
            </author>
            <editor role="depositor">              <persName>                <forename>Lydia</forename>
                <surname>Nelsom</surname>
              </persName>
              <email type="md5">bba8ce8b7a76814561866cfe35712816</email>
              <email type="domain">univ-amu.fr</email>
            </editor>
          </titleStmt>
          <editionStmt>            <edition n="v1" type="current">              <date type="whenSubmitted">2015-02-03 11:51:26</date>
              <date type="whenModified">2015-02-04 01:06:15</date>
              <date type="whenReleased">2015-02-03 11:51:26</date>
              <date type="whenProduced">2014-05</date>
            </edition>
            <respStmt>              <resp>contributor</resp>
              <name key="112288">                <persName>                  <forename>Lydia</forename>
                  <surname>Nelsom</surname>
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                <email type="md5">bba8ce8b7a76814561866cfe35712816</email>
                <email type="domain">univ-amu.fr</email>
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            <idno type="halBibtex">kozina:hal-01112598</idno>
            <idno type="halRefHtml">Journal of the Neurological Sciences, Elsevier, 2014, 340 ((1-2)), pp.198-207. <10.1016/j.jns.2014.03.028></idno>
            <idno type="halRef">Journal of the Neurological Sciences, Elsevier, 2014, 340 ((1-2)), pp.198-207. <10.1016/j.jns.2014.03.028></idno>
          </publicationStmt>
          <seriesStmt>            <idno type="stamp" n="CNRS">CNRS - Centre national de la recherche scientifique</idno>
            <idno type="stamp" n="UNIV-AMU">Aix Marseille Université</idno>
          </seriesStmt>
          <notesStmt>            <note type="audience" n="2">International</note>
            <note type="popular" n="0">No</note>
            <note type="peer" n="1">Yes</note>
          </notesStmt>
          <sourceDesc>            <biblStruct>              <analytic>                <title xml:lang="en">Tyrosine hydroxylase expression and activity in nigrostriatal dopaminergic neurons of MPTP-treated mice at the presymptomatic and symptomatic stages of parkinsonism</title>
                <author role="aut">                  <persName>                    <forename type="first">E.A.</forename>
                    <surname>Kozina</surname>
                  </persName>
                  <idno type="halauthorid">1124361</idno>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">GR</forename>
                    <surname>Khakimova</surname>
                  </persName>
                  <idno type="halauthorid">1124362</idno>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">V.G.</forename>
                    <surname>Khaindrava</surname>
                  </persName>
                  <idno type="halauthorid">1124363</idno>
                  <affiliation ref="#struct-199397"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">V.G.</forename>
                    <surname>Kucheryanu</surname>
                  </persName>
                  <idno type="halauthorid">1124364</idno>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">N.E.</forename>
                    <surname>Vorobyeva</surname>
                  </persName>
                  <idno type="halauthorid">1124365</idno>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">A.N.</forename>
                    <surname>Krasnov</surname>
                  </persName>
                  <idno type="halauthorid">273681</idno>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">S.G.</forename>
                    <surname>Georgieva</surname>
                  </persName>
                  <idno type="halauthorid">1124366</idno>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">L.</forename>
                    <surname>Kerkerian-Legoff</surname>
                  </persName>
                  <idno type="halauthorid">869023</idno>
                  <affiliation ref="#struct-199397"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">M.V.</forename>
                    <surname>Ugrumov</surname>
                  </persName>
                  <idno type="halauthorid">141052</idno>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">16375</idno>
                <idno type="issn">0022-510X</idno>
                <title level="j">Journal of the Neurological Sciences</title>
                <imprint>                  <publisher>Elsevier</publisher>
                  <biblScope unit="volume">340</biblScope>
                  <biblScope unit="issue">(1-2)</biblScope>
                  <biblScope unit="pp">198-207</biblScope>
                  <date type="datePub">2014-05</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1016/j.jns.2014.03.028</idno>
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          <profileDesc>            <langUsage>              <language ident="en">English</language>
            </langUsage>
            <textClass>              <classCode scheme="halDomain" n="sdv.bc">Life Sciences [q-bio]/Cellular Biology</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
            </textClass>
            <abstract xml:lang="en">Progressive degeneration of nigrostriatal dopaminergic (DA-ergic) neurons is a key component in the pathogenesis of Parkinson's disease, which develops for a long time at the preclinical stage with no motor dysfunctions due to the initiation of compensatory processes. The goal of this study was to evaluate the changes in surviving nigrostriatal DA-ergic neurons with focus on tyrosine hydroxylase (TH) in MPTP-treated mice at the presymptomatic and early symptomatic stages of parkinsonism. According to our data, a partial degeneration of DA-ergic neurons at the presymptomatic stage was accompanied by: (i) no change in TH mRNA content in the substantia nigra (SN) suggesting a compensatory increase of TH gene expression in individual neurons; (ii) a decrease of TH protein content in the nigrostriatal system and no change in individual neurons, suggesting a slowdown of TH translation. When comparing DA-ergic neurons at the early symptomatic stage and presymptomatic stage, it becomes evident: (i) a decrease of TH mRNA content in the SN and hence gene expression in individual neurons; (ii) a decrease of TH content in the striatum and its increase in the SN and individual neurons suggesting an acceleration of TH translation. TH activity, an index of the rate of DA synthesis, was unchanged in the SN and decreased in the striatum to the same degree at both stages of parkinsonism. In the meantime, TH activity in individual neurons appeared to be compensatory increased, but to a higher degree at the symptomatic stage than at the presymptomatic one. These data first show that DA depletion, which provokes motor dysfunction, is not a result of the decrease of TH activity and the rate of DA synthesis but is rather related to either a decrease of DA release or an increase of DA uptake in striatal DA-ergic axons.Copyright © 2014 Elsevier B.V. All rights reserved.</abstract>
          </profileDesc>
        </hal>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Tyrosine hydroxylase expression and activity in nigrostriatal dopaminergic neurons of MPTP-treated mice at the presymptomatic and symptomatic stages of parkinsonism

Tyrosine hydroxylase expression and activity in nigrostriatal dopaminergic neurons of MPTP-treated mice at the presymptomatic and symptomatic stages of parkinsonism

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