ParkinsonFranceV1, Hal, Curation, bibRecord, 000980

Synapto-protective drugs evaluation in reconstructed neuronal network

Identifieur interne : 000980 ( Hal/Curation ); précédent : 000979; suivant : 000981

Synapto-protective drugs evaluation in reconstructed neuronal network

Auteurs : Bérangère Deleglise [France] ; Benjamin Lassus [France] ; Vanessa Soubeyre [France] ; Aurélie Alleaume-Butaux [France] ; Johannes J. Hjorth [Pays-Bas] ; Maeva Vignes [France] ; Benoit Schneider [France] ; Bernard Brugg [France] ; Jean-Louis Viovy [France] ; Jean-Michel Peyrin [France]

Source :

PLoS ONE [ 1932-6203 ] ; 2013.

RBID : Hal:hal-01221378

Abstract

Chronic neurodegenerative syndromes such as Alzheimer’s and Parkinson’s diseases, or acute syndromes such as ischemic stroke or traumatic brain injuries are characterized by early synaptic collapse which precedes axonal and neuronal cell body degeneration and promotes early cognitive impairment in patients. Until now, neuroprotective strategies have failed to impede the progression of neurodegenerative syndromes. Drugs preventing the loss of cell body do not prevent the cognitive decline, probably because they lack synapto-protective effects. The absence of physiologically realistic neuronal network models which can be easily handled has hindered the development of synapto-protective drugs suitable for therapies. Here we describe a new microfluidic platform which makes it possible to study the consequences of axonal trauma of reconstructed oriented mouse neuronal networks. Each neuronal population and sub-compartment can be chemically addressed individually. The somatic, mid axon, presynaptic and postsynaptic effects of local pathological stresses or putative protective molecules can thus be evaluated with the help of this versatile “brain on chip” platform. We show that presynaptic loss is the earliest event observed following axotomy of cortical fibers, before any sign of axonal fragmentation or post-synaptic spine alteration. This platform can be used to screen and evaluate the synapto-protective potential of several drugs. For instance, NAD+ and the Rho-kinase inhibitor Y27632 can efficiently prevent synaptic disconnection, whereas the broad-spectrum caspase inhibitor zVAD-fmk and the stilbenoid resveratrol do not prevent presynaptic degeneration. Hence, this platform is a promising tool for fundamental research in the field of developmental and neurodegenerative neurosciences, and also offers the opportunity to set up pharmacological screening of axon-protective and synapto-protective drugs.

Url:

https://hal.archives-ouvertes.fr/hal-01221378

DOI: 10.1371/journal.pone.0071103

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<front><div type="abstract" xml:lang="en">Chronic neurodegenerative syndromes such as Alzheimer’s and Parkinson’s diseases, or acute syndromes such as ischemic stroke or traumatic brain injuries are characterized by early synaptic collapse which precedes axonal and neuronal cell body degeneration and promotes early cognitive impairment in patients. Until now, neuroprotective strategies have failed to impede the progression of neurodegenerative syndromes. Drugs preventing the loss of cell body do not prevent the cognitive decline, probably because they lack synapto-protective effects. The absence of physiologically realistic neuronal network models which can be easily handled has hindered the development of synapto-protective drugs suitable for therapies. Here we describe a new microfluidic platform which makes it possible to study the consequences of axonal trauma of reconstructed oriented mouse neuronal networks. Each neuronal population and sub-compartment can be chemically addressed individually. The somatic, mid axon, presynaptic and postsynaptic effects of local pathological stresses or putative protective molecules can thus be evaluated with the help of this versatile “brain on chip” platform. We show that presynaptic loss is the earliest event observed following axotomy of cortical fibers, before any sign of axonal fragmentation or post-synaptic spine alteration. This platform can be used to screen and evaluate the synapto-protective potential of several drugs. For instance, NAD+ and the Rho-kinase inhibitor Y27632 can efficiently prevent synaptic disconnection, whereas the broad-spectrum caspase inhibitor zVAD-fmk and the stilbenoid resveratrol do not prevent presynaptic degeneration. Hence, this platform is a promising tool for fundamental research in the field of developmental and neurodegenerative neurosciences, and also offers the opportunity to set up pharmacological screening of axon-protective and synapto-protective drugs.</div>
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            <author role="aut">              <persName>                <forename type="first">Benoit</forename>
                <surname>Schneider</surname>
              </persName>
              <idno type="halauthorid">1239262</idno>
              <affiliation ref="#struct-301361"></affiliation>
            </author>
            <author role="aut">              <persName>                <forename type="first">Bernard</forename>
                <surname>Brugg</surname>
              </persName>
              <idno type="halauthorid">156468</idno>
              <affiliation ref="#struct-479809"></affiliation>
            </author>
            <author role="aut">              <persName>                <forename type="first">Jean-Louis</forename>
                <surname>Viovy</surname>
              </persName>
              <idno type="halauthorid">118899</idno>
              <affiliation ref="#struct-440815"></affiliation>
            </author>
            <author role="crp">              <persName>                <forename type="first">Jean-Michel</forename>
                <surname>Peyrin</surname>
              </persName>
              <email type="md5">72dfe6bfc4b064476802d66a93ef513b</email>
              <email type="domain">upmc.fr</email>
              <idno type="halauthorid">1239263</idno>
              <affiliation ref="#struct-479809"></affiliation>
            </author>
            <editor role="depositor">              <persName>                <forename>Archive Ouverte</forename>
                <surname>ProdInra</surname>
              </persName>
              <email type="md5">859d2cba2c64f5bbc2add42f2b9992d1</email>
              <email type="domain">inra.fr</email>
            </editor>
            <funder>the French Research National Agency “Agence Nationale de la Recherche,” ANR RPIB “Neuroscreen” and ANR “PrionsensiTNF"</funder>
          </titleStmt>
          <editionStmt>            <edition n="v1" type="current">              <date type="whenSubmitted">2015-10-27 20:23:17</date>
              <date type="whenModified">2017-02-02 16:02:33</date>
              <date type="whenReleased">2015-10-28 14:40:16</date>
              <date type="whenProduced">2013</date>
              <date type="whenEndEmbargoed">2015-10-28</date>
              <ref type="file" target="https://hal.archives-ouvertes.fr/hal-01221378/document">                <date notBefore="2015-10-28"></date>
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              <ref type="file" subtype="publisherAgreement" n="1" target="https://hal.archives-ouvertes.fr/hal-01221378/file/2013_Deleglise_Plos%20One_%7BAE8659D7-9DFA-463F-BB85-41A72E751883%7D.pdf">                <date notBefore="2015-10-28"></date>
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            <respStmt>              <resp>contributor</resp>
              <name key="132775">                <persName>                  <forename>Archive Ouverte</forename>
                  <surname>ProdInra</surname>
                </persName>
                <email type="md5">859d2cba2c64f5bbc2add42f2b9992d1</email>
                <email type="domain">inra.fr</email>
              </name>
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          </editionStmt>
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            <idno type="halId">hal-01221378</idno>
            <idno type="halUri">https://hal.archives-ouvertes.fr/hal-01221378</idno>
            <idno type="halBibtex">deleglise:hal-01221378</idno>
            <idno type="halRefHtml">PLoS ONE, Public Library of Science, 2013, 8 (8), pp.1-9. <10.1371/journal.pone.0071103></idno>
            <idno type="halRef">PLoS ONE, Public Library of Science, 2013, 8 (8), pp.1-9. <10.1371/journal.pone.0071103></idno>
          </publicationStmt>
          <seriesStmt>            <idno type="stamp" n="CNRS">CNRS - Centre national de la recherche scientifique</idno>
            <idno type="stamp" n="INRA">INRA - Institut national de la recherche agronomique</idno>
            <idno type="stamp" n="UNIV-PARIS5">Université Paris Descartes (Paris 5)</idno>
            <idno type="stamp" n="PSL">Paris Sciences et Lettres (PSL) Research University</idno>
            <idno type="stamp" n="UPMC">Université Pierre et Marie Curie</idno>
            <idno type="stamp" n="CURIE" p="FNCLCC">Institut Curie</idno>
            <idno type="stamp" n="PCC_UMR168" p="UPMC">Physico-Chimie Curie</idno>
            <idno type="stamp" n="FNCLCC" p="INSERM">UNICANCER</idno>
            <idno type="stamp" n="USPC">Université Sorbonne Paris Cité</idno>
            <idno type="stamp" n="AGREENIUM">Archive ouverte en agrobiosciences</idno>
          </seriesStmt>
          <notesStmt>            <note type="audience" n="1">Not set</note>
            <note type="popular" n="0">No</note>
            <note type="peer" n="1">Yes</note>
          </notesStmt>
          <sourceDesc>            <biblStruct>              <analytic>                <title xml:lang="en">Synapto-protective drugs evaluation in reconstructed neuronal network</title>
                <author role="aut">                  <persName>                    <forename type="first">Bérangère</forename>
                    <surname>Deleglise</surname>
                  </persName>
                  <idno type="halauthorid">1239238</idno>
                  <affiliation ref="#struct-440810"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Benjamin</forename>
                    <surname>Lassus</surname>
                  </persName>
                  <idno type="halauthorid">1239259</idno>
                  <affiliation ref="#struct-479809"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Vanessa</forename>
                    <surname>Soubeyre</surname>
                  </persName>
                  <idno type="halauthorid">1239241</idno>
                  <affiliation ref="#struct-479809"></affiliation>
                  <affiliation ref="#struct-440796"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Aurélie</forename>
                    <surname>Alleaume-Butaux</surname>
                  </persName>
                  <idno type="halauthorid">1239260</idno>
                  <affiliation ref="#struct-440811"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Johannes J.</forename>
                    <surname>Hjorth</surname>
                  </persName>
                  <idno type="halauthorid">1239261</idno>
                  <affiliation ref="#struct-440814"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Maeva</forename>
                    <surname>Vignes</surname>
                  </persName>
                  <idno type="halauthorid">1239242</idno>
                  <affiliation ref="#struct-479809"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Benoit</forename>
                    <surname>Schneider</surname>
                  </persName>
                  <idno type="halauthorid">1239262</idno>
                  <affiliation ref="#struct-301361"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Bernard</forename>
                    <surname>Brugg</surname>
                  </persName>
                  <idno type="halauthorid">156468</idno>
                  <affiliation ref="#struct-479809"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Jean-Louis</forename>
                    <surname>Viovy</surname>
                  </persName>
                  <idno type="halauthorid">118899</idno>
                  <affiliation ref="#struct-440815"></affiliation>
                </author>
                <author role="crp">                  <persName>                    <forename type="first">Jean-Michel</forename>
                    <surname>Peyrin</surname>
                  </persName>
                  <email type="md5">72dfe6bfc4b064476802d66a93ef513b</email>
                  <email type="domain">upmc.fr</email>
                  <idno type="halauthorid">1239263</idno>
                  <affiliation ref="#struct-479809"></affiliation>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">28700</idno>
                <idno type="issn">1932-6203</idno>
                <title level="j">PLoS ONE</title>
                <imprint>                  <publisher>Public Library of Science</publisher>
                  <biblScope unit="volume">8</biblScope>
                  <biblScope unit="issue">8</biblScope>
                  <biblScope unit="pp">1-9</biblScope>
                  <date type="datePub">2013</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1371/journal.pone.0071103</idno>
              <idno type="prodinra">329668</idno>
              <idno type="pubmed">23976987</idno>
            </biblStruct>
          </sourceDesc>
          <profileDesc>            <langUsage>              <language ident="en">English</language>
            </langUsage>
            <textClass>              <classCode scheme="halDomain" n="sdv.mhep">Life Sciences [q-bio]/Human health and pathology</classCode>
              <classCode scheme="halDomain" n="sdv.neu">Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
            </textClass>
            <abstract xml:lang="en">Chronic neurodegenerative syndromes such as Alzheimer’s and Parkinson’s diseases, or acute syndromes such as ischemic stroke or traumatic brain injuries are characterized by early synaptic collapse which precedes axonal and neuronal cell body degeneration and promotes early cognitive impairment in patients. Until now, neuroprotective strategies have failed to impede the progression of neurodegenerative syndromes. Drugs preventing the loss of cell body do not prevent the cognitive decline, probably because they lack synapto-protective effects. The absence of physiologically realistic neuronal network models which can be easily handled has hindered the development of synapto-protective drugs suitable for therapies. Here we describe a new microfluidic platform which makes it possible to study the consequences of axonal trauma of reconstructed oriented mouse neuronal networks. Each neuronal population and sub-compartment can be chemically addressed individually. The somatic, mid axon, presynaptic and postsynaptic effects of local pathological stresses or putative protective molecules can thus be evaluated with the help of this versatile “brain on chip” platform. We show that presynaptic loss is the earliest event observed following axotomy of cortical fibers, before any sign of axonal fragmentation or post-synaptic spine alteration. This platform can be used to screen and evaluate the synapto-protective potential of several drugs. For instance, NAD+ and the Rho-kinase inhibitor Y27632 can efficiently prevent synaptic disconnection, whereas the broad-spectrum caspase inhibitor zVAD-fmk and the stilbenoid resveratrol do not prevent presynaptic degeneration. Hence, this platform is a promising tool for fundamental research in the field of developmental and neurodegenerative neurosciences, and also offers the opportunity to set up pharmacological screening of axon-protective and synapto-protective drugs.</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)

Synapto-protective drugs evaluation in reconstructed neuronal network

Synapto-protective drugs evaluation in reconstructed neuronal network

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