ParkinsonFranceV1, Hal, Corpus, bibRecord, 000348

Early prenatal exposure to MPTP does not affect nigrostrial neurons in macaque monkey

Identifieur interne : 000348 ( Hal/Corpus ); précédent : 000347; suivant : 000349

Early prenatal exposure to MPTP does not affect nigrostrial neurons in macaque monkey

Auteurs : Mathieu Bourdenx ; Sandra Dovero ; Philippe De Deurwaerdère ; Qin Li ; Erwan Bezard

Source :

Synapse [ 0887-4476 ] ; 2016-02.

RBID : Hal:hal-01286262

Abstract

The discovery of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin that induces parkinsonism in both human and primate, has prompted the search for environmental toxins potentially responsible for idiopathic Parkinson's disease (PD). The present study reports the ultimate effects of MPTP intoxication of a female macaque monkey, which unraveled to be pregnant after parkinsonism had developed, upon its fetus. Detailed examination of the offpsring nigrostriatal pathway showed that tyrosine hydroxylase immunoreactivity in caudate-putamen nuclei and substantia nigra compacta (SNc) was not different from an age-matched control. Biochemical analysis of the tissue content of dopaminergic markers further suggested modification of metabolism in the MPTP-exposed monkey. These data suggest that early prenatal intoxication does not destroy nigrostriatal neurons, most likely because dopamine neurons had not developed yet when exposed to MPTP. Synapse 70:52-56, 2016. © 2015 Wiley Periodicals, Inc.

Url:

https://hal.archives-ouvertes.fr/hal-01286262

DOI: 10.1002/syn.21876

Links to Exploration step

Hal:hal-01286262

Le document en format XML

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<front><div type="abstract" xml:lang="en">The discovery of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin that induces parkinsonism in both human and primate, has prompted the search for environmental toxins potentially responsible for idiopathic Parkinson's disease (PD). The present study reports the ultimate effects of MPTP intoxication of a female macaque monkey, which unraveled to be pregnant after parkinsonism had developed, upon its fetus. Detailed examination of the offpsring nigrostriatal pathway showed that tyrosine hydroxylase immunoreactivity in caudate-putamen nuclei and substantia nigra compacta (SNc) was not different from an age-matched control. Biochemical analysis of the tissue content of dopaminergic markers further suggested modification of metabolism in the MPTP-exposed monkey. These data suggest that early prenatal intoxication does not destroy nigrostriatal neurons, most likely because dopamine neurons had not developed yet when exposed to MPTP. Synapse 70:52-56, 2016. © 2015 Wiley Periodicals, Inc. </div>
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                <author role="aut">                  <persName>                    <forename type="first">Qin</forename>
                    <surname>Li</surname>
                  </persName>
                  <idno type="halauthorid">224848</idno>
                  <affiliation ref="#struct-439190"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Erwan</forename>
                    <surname>Bezard</surname>
                  </persName>
                  <idno type="halauthorid">537314</idno>
                  <affiliation ref="#struct-439125"></affiliation>
                  <affiliation ref="#struct-244085"></affiliation>
                </author>
              </analytic>
              <monogr>                <idno type="halJournalId" status="VALID">19270</idno>
                <idno type="issn">0887-4476</idno>
                <idno type="eissn">1098-2396</idno>
                <title level="j">Synapse</title>
                <imprint>                  <publisher>Wiley-Blackwell</publisher>
                  <biblScope unit="volume">70</biblScope>
                  <biblScope unit="issue">2</biblScope>
                  <date type="datePub">2016-02</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1002/syn.21876</idno>
              <idno type="pubmed">26584009</idno>
            </biblStruct>
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          <profileDesc>            <langUsage>              <language ident="en">English</language>
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            <textClass>              <classCode scheme="halDomain" n="sdv">Life Sciences [q-bio]</classCode>
              <classCode scheme="halTypology" n="ART">Journal articles</classCode>
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            <abstract xml:lang="en">The discovery of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin that induces parkinsonism in both human and primate, has prompted the search for environmental toxins potentially responsible for idiopathic Parkinson's disease (PD). The present study reports the ultimate effects of MPTP intoxication of a female macaque monkey, which unraveled to be pregnant after parkinsonism had developed, upon its fetus. Detailed examination of the offpsring nigrostriatal pathway showed that tyrosine hydroxylase immunoreactivity in caudate-putamen nuclei and substantia nigra compacta (SNc) was not different from an age-matched control. Biochemical analysis of the tissue content of dopaminergic markers further suggested modification of metabolism in the MPTP-exposed monkey. These data suggest that early prenatal intoxication does not destroy nigrostriatal neurons, most likely because dopamine neurons had not developed yet when exposed to MPTP. Synapse 70:52-56, 2016. © 2015 Wiley Periodicals, Inc. </abstract>
          </profileDesc>
        </hal>
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	La maladie de Parkinson en France (serveur d'exploration)
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Early prenatal exposure to MPTP does not affect nigrostrial neurons in macaque monkey

Early prenatal exposure to MPTP does not affect nigrostrial neurons in macaque monkey

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