Caspase‐3 activation in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mice
Identifieur interne : 004850 ( Main/Exploration ); précédent : 004849; suivant : 004851Caspase‐3 activation in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mice
Auteurs : Hélène Turmel [France] ; Andreas Hartmann [France] ; Karine Parain [France] ; Aicha Douhou [France] ; Anu Srinivasan [États-Unis] ; Yves Agid [France] ; Etienne C. Hirsch [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2001-03.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (administration & dosage), 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), Animal, Animal model, Animals, Apoptosis, Apoptosis (drug effects), Caspase 3, Caspases (metabolism), Disease Models, Animal, Dopamine Agents (administration & dosage), Dopamine Agents (adverse effects), Enzymatic activity, Immunohistochemistry, MPP+, MPTP, Male, Mice, Mice, Inbred C57BL, Mouse, Neurons (drug effects), Neurons (enzymology), Neurons (pathology), Parkinson Disease, Secondary (chemically induced), Parkinson disease, Parkinson's disease, Pathogenesis, Substantia Nigra (drug effects), Substantia Nigra (enzymology), Tyrosine 3-Monooxygenase (metabolism), apoptosis, caspase‐3.
- MESH :
- chemical , administration & dosage : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents.
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Apoptosis, Neurons, Substantia Nigra.
- enzymology : Neurons, Substantia Nigra.
- chemical , metabolism : Caspases, Tyrosine 3-Monooxygenase.
- pathology : Neurons.
- Animals, Caspase 3, Disease Models, Animal, Immunohistochemistry, Male, Mice, Mice, Inbred C57BL.
Abstract
In 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1‐methyl‐4‐phenylpyridinium (MPP+) may be mediated by caspase‐3. To establish whether caspase‐3 activation may indeed play a role in an in vivo model of PD, we studied caspase‐3 activation in C57Bl/6 mice subchronically intoxicated with MPTP. We show that caspase‐3 activation peaks early, at days 1 and 2 after the end of MPTP intoxication. In contrast, pycnotic neurons persist until day 7 postintoxication, indicating that caspase‐3 activation is an early and transient phenomenon in apoptotic death of DA neurons. We further demonstrate that loss of tyrosine hydroxylase (TH) immunoreactivity in this model is indeed due to cell loss rather than to loss of TH protein expression. We conclude that mice subchronically intoxicated with MPTP represent a valid PD model to study and manipulate caspase activation in vivo. © 2001 Movement Disorder Society.
Url:
DOI: 10.1002/mds.1037
Affiliations:
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Hirsch</name><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>INSERM U 289, Hópital de la Salpétrière, Paris</wicri:regionArea><placeName><settlement type="city">Paris</settlement></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2001-03">2001-03</date><biblScope unit="vol">16</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="185">185</biblScope><biblScope unit="page" to="189">189</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">919388BA1F3FE05BB4D9DE7516DA1DB6A839064B</idno><idno type="DOI">10.1002/mds.1037</idno><idno type="ArticleID">MDS1037</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (administration & dosage)</term><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects)</term><term>Animal</term><term>Animal model</term><term>Animals</term><term>Apoptosis</term><term>Apoptosis (drug effects)</term><term>Caspase 3</term><term>Caspases (metabolism)</term><term>Disease Models, Animal</term><term>Dopamine Agents (administration & dosage)</term><term>Dopamine Agents (adverse effects)</term><term>Enzymatic activity</term><term>Immunohistochemistry</term><term>MPP+</term><term>MPTP</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mouse</term><term>Neurons (drug effects)</term><term>Neurons (enzymology)</term><term>Neurons (pathology)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Pathogenesis</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (enzymology)</term><term>Tyrosine 3-Monooxygenase (metabolism)</term><term>apoptosis</term><term>caspase‐3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Dopamine Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Dopamine Agents</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Neurons</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Neurons</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Caspases</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Caspase 3</term><term>Disease Models, Animal</term><term>Immunohistochemistry</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Activité enzymatique</term><term>Animal</term><term>Apoptose</term><term>Caspase 3</term><term>Modèle animal</term><term>Parkinson maladie</term><term>Pathogénie</term><term>Souris</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1‐methyl‐4‐phenylpyridinium (MPP+) may be mediated by caspase‐3. To establish whether caspase‐3 activation may indeed play a role in an in vivo model of PD, we studied caspase‐3 activation in C57Bl/6 mice subchronically intoxicated with MPTP. We show that caspase‐3 activation peaks early, at days 1 and 2 after the end of MPTP intoxication. In contrast, pycnotic neurons persist until day 7 postintoxication, indicating that caspase‐3 activation is an early and transient phenomenon in apoptotic death of DA neurons. We further demonstrate that loss of tyrosine hydroxylase (TH) immunoreactivity in this model is indeed due to cell loss rather than to loss of TH protein expression. We conclude that mice subchronically intoxicated with MPTP represent a valid PD model to study and manipulate caspase activation in vivo. © 2001 Movement Disorder Society.</div></front></TEI><affiliations><list><country><li>France</li><li>États-Unis</li></country><region><li>Californie</li><li>Île-de-France</li></region><settlement><li>Paris</li></settlement><orgName><li>Hôpital de la Salpêtrière</li></orgName></list><tree><country name="France"><noRegion><name sortKey="Turmel, Helene" sort="Turmel, Helene" uniqKey="Turmel H" first="Hélène" last="Turmel">Hélène Turmel</name></noRegion><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><name sortKey="Douhou, Aicha" sort="Douhou, Aicha" uniqKey="Douhou A" first="Aicha" last="Douhou">Aicha Douhou</name><name sortKey="Hartmann, Andreas" sort="Hartmann, Andreas" uniqKey="Hartmann A" first="Andreas" last="Hartmann">Andreas Hartmann</name><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C." last="Hirsch">Etienne C. Hirsch</name><name sortKey="Parain, Karine" sort="Parain, Karine" uniqKey="Parain K" first="Karine" last="Parain">Karine Parain</name></country><country name="États-Unis"><region name="Californie"><name sortKey="Srinivasan, Anu" sort="Srinivasan, Anu" uniqKey="Srinivasan A" first="Anu" last="Srinivasan">Anu Srinivasan</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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