ParkinsonFranceV1, Hal, Checkpoint, bibRecord, 000559

High frequency stimulation of the subthalamic nucleus impacts adult neurogenesis in a rat model of Parkinson's disease.

Identifieur interne : 000559 ( Hal/Checkpoint ); précédent : 000558; suivant : 000560

High frequency stimulation of the subthalamic nucleus impacts adult neurogenesis in a rat model of Parkinson's disease.

Auteurs : Vitaly Khaindrava [France] ; Pascal Salin [France] ; Christophe Melon [France] ; Michael Ugrumov ; Lydia Kerkerian-Le-Goff [France] ; Annie Daszuta [France]

Source :

Neurobiology of Disease [ 0969-9961 ] ; 2011-06.

RBID : Hal:hal-00848858

Abstract

Chronic high frequency stimulation of the subthalamic nucleus (STN-HFS) efficiently alleviates motor symptoms of advanced Parkinson's disease (PD). Here, we looked for possible STN-HFS-induced changes on adult brain neurogenesis in the hippocampus and olfactory bulb that may be related to non-motor deficits associated to PD, such as mood disorders and olfaction deficits. Cell proliferation (Ki-67 immuno-positive-cells) and survival (bromodeoxyuridine (BrdU)-immuno-positive cells) were assessed in the subventricular zone-olfactory bulb continuum and the dentate gyrus of the hippocampus of hemiparkinsonian rats with or without continuous STN-HFS for 8 days. Dopamine lesion impaired cell proliferation and survival through different mechanisms, the effect on proliferation being correlated to the level of dopamine depletion whereas the effect on survival was not. Prolonged STN-HFS did not affect cell proliferation, but increased cell survival bilaterally. In these regions of constitutive neurogenesis, the percentage of new neuroblasts (BrdU-doublecortin-positive cells) was unchanged, suggesting that STN-HFS can lead to a net increase in newly formed neurons later on. STN-HFS also increased new cell survival in the striatum and promoted dopamine system recovery detected by tyrosine hydroxylase immunostaining. These data provide the first evidence that prolonged STN-HFS has a neurorestorative action and support the view that the action of this neurosurgical treatment can bypass the cortico-basal ganglia-thalamocortical loop circuits and largely impinge neuroplasticity and brain function.

Url:

https://hal.archives-ouvertes.fr/hal-00848858

DOI: 10.1016/j.nbd.2011.01.018

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Le document en format XML

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<author><name sortKey="Daszuta, Annie" sort="Daszuta, Annie" uniqKey="Daszuta A" first="Annie" last="Daszuta">Annie Daszuta</name>
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<idno type="DOI">10.1016/j.nbd.2011.01.018</idno>
<series><title level="j">Neurobiology of Disease</title>
<idno type="ISSN">0969-9961</idno>
<imprint><date type="datePub">2011-06</date>
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<front><div type="abstract" xml:lang="en">Chronic high frequency stimulation of the subthalamic nucleus (STN-HFS) efficiently alleviates motor symptoms of advanced Parkinson's disease (PD). Here, we looked for possible STN-HFS-induced changes on adult brain neurogenesis in the hippocampus and olfactory bulb that may be related to non-motor deficits associated to PD, such as mood disorders and olfaction deficits. Cell proliferation (Ki-67 immuno-positive-cells) and survival (bromodeoxyuridine (BrdU)-immuno-positive cells) were assessed in the subventricular zone-olfactory bulb continuum and the dentate gyrus of the hippocampus of hemiparkinsonian rats with or without continuous STN-HFS for 8 days. Dopamine lesion impaired cell proliferation and survival through different mechanisms, the effect on proliferation being correlated to the level of dopamine depletion whereas the effect on survival was not. Prolonged STN-HFS did not affect cell proliferation, but increased cell survival bilaterally. In these regions of constitutive neurogenesis, the percentage of new neuroblasts (BrdU-doublecortin-positive cells) was unchanged, suggesting that STN-HFS can lead to a net increase in newly formed neurons later on. STN-HFS also increased new cell survival in the striatum and promoted dopamine system recovery detected by tyrosine hydroxylase immunostaining. These data provide the first evidence that prolonged STN-HFS has a neurorestorative action and support the view that the action of this neurosurgical treatment can bypass the cortico-basal ganglia-thalamocortical loop circuits and largely impinge neuroplasticity and brain function.</div>
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            <author role="aut">              <persName>                <forename type="first">Vitaly</forename>
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            <author role="aut">              <persName>                <forename type="first">Pascal</forename>
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            <author role="aut">              <persName>                <forename type="first">Christophe</forename>
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            <editor role="depositor">              <persName>                <forename>Lydia</forename>
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              <date type="whenModified">2013-07-29 14:08:58</date>
              <date type="whenReleased">2013-07-29 14:08:58</date>
              <date type="whenProduced">2011-06</date>
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          <sourceDesc>            <biblStruct>              <analytic>                <title xml:lang="en">High frequency stimulation of the subthalamic nucleus impacts adult neurogenesis in a rat model of Parkinson's disease.</title>
                <author role="aut">                  <persName>                    <forename type="first">Vitaly</forename>
                    <surname>Khaindrava</surname>
                  </persName>
                  <idno type="halauthorid">874362</idno>
                  <affiliation ref="#struct-199397"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Pascal</forename>
                    <surname>Salin</surname>
                  </persName>
                  <idno type="halauthorid">410384</idno>
                  <affiliation ref="#struct-199397"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Christophe</forename>
                    <surname>Melon</surname>
                  </persName>
                  <idno type="halauthorid">410379</idno>
                  <affiliation ref="#struct-199397"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Michael</forename>
                    <surname>Ugrumov</surname>
                  </persName>
                  <idno type="halauthorid">874363</idno>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Lydia</forename>
                    <surname>Kerkerian-Le-Goff</surname>
                  </persName>
                  <idno type="halauthorid">874364</idno>
                  <affiliation ref="#struct-199397"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Annie</forename>
                    <surname>Daszuta</surname>
                  </persName>
                  <idno type="halauthorid">120674</idno>
                  <affiliation ref="#struct-199397"></affiliation>
                  <affiliation ref="#struct-876"></affiliation>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">13277</idno>
                <idno type="issn">0969-9961</idno>
                <idno type="eissn">1095-953X</idno>
                <title level="j">Neurobiology of Disease</title>
                <imprint>                  <publisher>Elsevier</publisher>
                  <biblScope unit="volume">42</biblScope>
                  <biblScope unit="issue">3</biblScope>
                  <biblScope unit="pp">284-91</biblScope>
                  <date type="datePub">2011-06</date>
                  <date type="dateEpub">2011-02-03</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1016/j.nbd.2011.01.018</idno>
              <idno type="pubmed">21296669</idno>
            </biblStruct>
          </sourceDesc>
          <profileDesc>            <langUsage>              <language ident="en">English</language>
            </langUsage>
            <textClass>              <classCode scheme="mesh">Analysis of Variance</classCode>
              <classCode scheme="mesh">Animals</classCode>
              <classCode scheme="mesh">Rats</classCode>
              <classCode scheme="mesh">Rats, Wistar</classCode>
              <classCode scheme="mesh">Subthalamic Nucleus</classCode>
              <classCode scheme="mesh">Deep Brain Stimulation</classCode>
              <classCode scheme="mesh">Disease Models, Animal</classCode>
              <classCode scheme="mesh">Dopamine</classCode>
              <classCode scheme="mesh">Electrodes, Implanted</classCode>
              <classCode scheme="mesh">Immunohistochemistry</classCode>
              <classCode scheme="mesh">Male</classCode>
              <classCode scheme="mesh">Neurogenesis</classCode>
              <classCode scheme="mesh">Parkinson Disease</classCode>
              <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">Chronic high frequency stimulation of the subthalamic nucleus (STN-HFS) efficiently alleviates motor symptoms of advanced Parkinson's disease (PD). Here, we looked for possible STN-HFS-induced changes on adult brain neurogenesis in the hippocampus and olfactory bulb that may be related to non-motor deficits associated to PD, such as mood disorders and olfaction deficits. Cell proliferation (Ki-67 immuno-positive-cells) and survival (bromodeoxyuridine (BrdU)-immuno-positive cells) were assessed in the subventricular zone-olfactory bulb continuum and the dentate gyrus of the hippocampus of hemiparkinsonian rats with or without continuous STN-HFS for 8 days. Dopamine lesion impaired cell proliferation and survival through different mechanisms, the effect on proliferation being correlated to the level of dopamine depletion whereas the effect on survival was not. Prolonged STN-HFS did not affect cell proliferation, but increased cell survival bilaterally. In these regions of constitutive neurogenesis, the percentage of new neuroblasts (BrdU-doublecortin-positive cells) was unchanged, suggesting that STN-HFS can lead to a net increase in newly formed neurons later on. STN-HFS also increased new cell survival in the striatum and promoted dopamine system recovery detected by tyrosine hydroxylase immunostaining. These data provide the first evidence that prolonged STN-HFS has a neurorestorative action and support the view that the action of this neurosurgical treatment can bypass the cortico-basal ganglia-thalamocortical loop circuits and largely impinge neuroplasticity and brain function.</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)

High frequency stimulation of the subthalamic nucleus impacts adult neurogenesis in a rat model of Parkinson's disease.

High frequency stimulation of the subthalamic nucleus impacts adult neurogenesis in a rat model of Parkinson's disease.

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