Neuronal protective and rescue effects of deprenyl against MPP+ dopaminergic toxicity
Identifieur interne : 002306 ( Main/Exploration ); précédent : 002305; suivant : 002307Neuronal protective and rescue effects of deprenyl against MPP+ dopaminergic toxicity
Auteurs : -M. Wu [États-Unis, Taïwan] ; L. Murphy [États-Unis] ; C. Chiueh [États-Unis]Source :
- Journal of Neural Transmission / General Section JNT [ 0300-9564 ] ; 1995-02-01.
Abstract
Summary: Intranigral infusion of 1-Methyl-4-phenylpyridinium ion (MPP+, 2.1–16.8 nmol) dose-dependently injured nigral neurons as reflected by reduced dopamine levels in the ipsilateral striatum four days after the infusion of this toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Coadministration of deprenyl (4.2 nmol) with MPP+ into the substantia nigra protected against MPP+-induced moderate (20–50%) but not severe (over 70%) nigral injury as reflected in striatal dopamine reductions. However, supplementary treatment with deprenyl (0.25 mg/kg, s.c., twice daily for 4 days) after intranigral infusion of MPP+ significantly rescued nigral neurons from more severe damage caused by a higher MPP+ does (8.4 nmol) manifested by a lesser striatal dopamine decrease (−31%) compared to the non-deprenyl treated group (−70%). Thus, in addition to the blockade of bioactivation of MPTP, deprenyl can protect and/or rescue nigral neurons from MPP+-induced dopaminergic neurotoxicity. These in vivo data add further evidence to suggest that deprenyl, a putative and clinically unproven neuroprotective agent, may be of value in slowing the progressive nigral degeneration in “early” Parkinson's disease, but may prove to be less so in its terminal stages.
Url:
DOI: 10.1007/BF01276865
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Chiueh</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:86B5714BB8816374643E664DBAC8247692E9FAB3</idno><date when="1995" year="1995">1995</date><idno type="doi">10.1007/BF01276865</idno><idno type="url">https://api.istex.fr/document/86B5714BB8816374643E664DBAC8247692E9FAB3/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000910</idno><idno type="wicri:Area/Main/Curation">000793</idno><idno type="wicri:Area/Main/Exploration">002306</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neuronal protective and rescue effects of deprenyl against MPP+ dopaminergic toxicity</title><author><name sortKey="Wu, M" sort="Wu, M" uniqKey="Wu " first="-M." last="Wu">-M. Wu</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Unit on Neurotoxicology and Neuroprotection, Laboratory of Clinical Science, National Institute of Mental Health, NIH Clinical Center 10/3D-41, Bethesda, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, National Taiwan University Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Murphy, L" sort="Murphy, L" uniqKey="Murphy L" first="L." last="Murphy">L. Murphy</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Section on Clinical Neuropharmacology, Laboratory of Clinical Science, National Institute of Mental Health, NIH Clinical Center 10/3D-41, Bethesda, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Chiueh, C" sort="Chiueh, C" uniqKey="Chiueh C" first="C." last="Chiueh">C. Chiueh</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Unit on Neurotoxicology and Neuroprotection, Laboratory of Clinical Science, National Institute of Mental Health, NIH Clinical Center 10/3D-41, Bethesda, Maryland</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neural Transmission / General Section JNT</title><title level="j" type="abbrev">J. Neural Transmission</title><idno type="ISSN">0300-9564</idno><idno type="eISSN">1435-1463</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1995-02-01">1995-02-01</date><biblScope unit="volume">100</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="53">53</biblScope><biblScope unit="page" to="61">61</biblScope></imprint><idno type="ISSN">0300-9564</idno></series><idno type="istex">86B5714BB8816374643E664DBAC8247692E9FAB3</idno><idno type="DOI">10.1007/BF01276865</idno><idno type="ArticleID">Art6</idno><idno type="ArticleID">BF01276865</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0300-9564</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Intranigral infusion of 1-Methyl-4-phenylpyridinium ion (MPP+, 2.1–16.8 nmol) dose-dependently injured nigral neurons as reflected by reduced dopamine levels in the ipsilateral striatum four days after the infusion of this toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Coadministration of deprenyl (4.2 nmol) with MPP+ into the substantia nigra protected against MPP+-induced moderate (20–50%) but not severe (over 70%) nigral injury as reflected in striatal dopamine reductions. However, supplementary treatment with deprenyl (0.25 mg/kg, s.c., twice daily for 4 days) after intranigral infusion of MPP+ significantly rescued nigral neurons from more severe damage caused by a higher MPP+ does (8.4 nmol) manifested by a lesser striatal dopamine decrease (−31%) compared to the non-deprenyl treated group (−70%). Thus, in addition to the blockade of bioactivation of MPTP, deprenyl can protect and/or rescue nigral neurons from MPP+-induced dopaminergic neurotoxicity. These in vivo data add further evidence to suggest that deprenyl, a putative and clinically unproven neuroprotective agent, may be of value in slowing the progressive nigral degeneration in “early” Parkinson's disease, but may prove to be less so in its terminal stages.</div></front></TEI><affiliations><list><country><li>Taïwan</li><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Wu, M" sort="Wu, M" uniqKey="Wu " first="-M." last="Wu">-M. Wu</name></region><name sortKey="Chiueh, C" sort="Chiueh, C" uniqKey="Chiueh C" first="C." last="Chiueh">C. Chiueh</name><name sortKey="Murphy, L" sort="Murphy, L" uniqKey="Murphy L" first="L." last="Murphy">L. Murphy</name></country><country name="Taïwan"><noRegion><name sortKey="Wu, M" sort="Wu, M" uniqKey="Wu " first="-M." last="Wu">-M. Wu</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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