A dopamine receptor contributes to paraquat-induced neurotoxicity in Drosophila
Identifieur interne : 000A74 ( Main/Exploration ); précédent : 000A73; suivant : 000A75A dopamine receptor contributes to paraquat-induced neurotoxicity in Drosophila
Auteurs : Marlène Cassar [France] ; Abdul-Raouf Issa [France] ; Thomas Riemensperger [France] ; Céline Petitgas [France] ; Thomas Rival [France] ; Hélène Coulom [France] ; Magali Iché-Torres [France] ; Kyung-An Han [États-Unis] ; Serge Birman [France]Source :
- Human Molecular Genetics [ 0964-6906 ] ; 2014.
English descriptors
- KwdEn :
- Age Factors, Animals, Disease Models, Animal, Dopamine (metabolism), Dopaminergic Neurons (metabolism), Drosophila Proteins (genetics), Drosophila Proteins (metabolism), Drosophila melanogaster (growth & development), Drosophila melanogaster (metabolism), Environmental Exposure, Female, Humans, Neurotoxicity Syndromes (metabolism), Paraquat (toxicity), Parkinson Disease, Receptors, Dopamine D1 (metabolism), Ryanodine Receptor Calcium Release Channel (genetics).
- MESH :
- chemical , genetics : Drosophila Proteins, Ryanodine Receptor Calcium Release Channel.
- chemical , metabolism : Dopamine, Drosophila Proteins, Receptors, Dopamine D1.
- growth & development : Drosophila melanogaster.
- metabolism : Dopaminergic Neurons, Drosophila melanogaster, Neurotoxicity Syndromes.
- chemical , toxicity : Paraquat.
- Age Factors, Animals, Disease Models, Animal, Environmental Exposure, Female, Humans, Parkinson Disease.
Abstract
Long-term exposure to environmental oxidative stressors, like the herbicide paraquat (PQ), has been linked to the development of Parkinson's disease (PD), the most frequent neurodegenerative movement disorder. Paraquat is thus frequently used in the fruit fly
Url:
DOI: 10.1093/hmg/ddu430
PubMed: 25158689
PubMed Central: 4326327
Affiliations:
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Le document en format XML
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<author><name sortKey="Han, Kyung An" sort="Han, Kyung An" uniqKey="Han K" first="Kyung-An" last="Han">Kyung-An Han</name>
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<term>Dopaminergic Neurons (metabolism)</term>
<term>Drosophila Proteins (genetics)</term>
<term>Drosophila Proteins (metabolism)</term>
<term>Drosophila melanogaster (growth & development)</term>
<term>Drosophila melanogaster (metabolism)</term>
<term>Environmental Exposure</term>
<term>Female</term>
<term>Humans</term>
<term>Neurotoxicity Syndromes (metabolism)</term>
<term>Paraquat (toxicity)</term>
<term>Parkinson Disease</term>
<term>Receptors, Dopamine D1 (metabolism)</term>
<term>Ryanodine Receptor Calcium Release Channel (genetics)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Drosophila Proteins</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term>
<term>Drosophila Proteins</term>
<term>Receptors, Dopamine D1</term>
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<front><div type="abstract" xml:lang="en"><p>Long-term exposure to environmental oxidative stressors, like the herbicide paraquat (PQ), has been linked to the development of Parkinson's disease (PD), the most frequent neurodegenerative movement disorder. Paraquat is thus frequently used in the fruit fly <italic>Drosophila melanogaster</italic>
and other animal models to study PD and the degeneration of dopaminergic neurons (DNs) that characterizes this disease. Here, we show that a D<sub>1</sub>
-like dopamine (DA) receptor, DAMB, actively contributes to the fast central nervous system (CNS) failure induced by PQ in the fly. First, we found that a long-term increase in neuronal DA synthesis reduced <italic>DAMB</italic>
expression and protected against PQ neurotoxicity. Secondly, a striking age-related decrease in PQ resistance in young adult flies correlated with an augmentation of <italic>DAMB</italic>
expression. This aging-associated increase in oxidative stress vulnerability was not observed in a <italic>DAMB</italic>
-deficient mutant. Thirdly, targeted inactivation of this receptor in glutamatergic neurons (GNs) markedly enhanced the survival of <italic>Drosophila</italic>
exposed to either PQ or neurotoxic levels of DA, whereas, conversely, <italic>DAMB</italic>
overexpression in these cells made the flies more vulnerable to both compounds. Fourthly, a mutation in the <italic>Drosophila</italic>
ryanodine receptor (<italic>RyR</italic>
), which inhibits activity-induced increase in cytosolic Ca<sup>2+</sup>
, also strongly enhanced PQ resistance. Finally, we found that <italic>DAMB</italic>
overexpression in specific neuronal populations arrested development of the fly and that <italic>in vivo</italic>
stimulation of either DNs or GNs increased PQ susceptibility. This suggests a model for DA receptor-mediated potentiation of PQ-induced neurotoxicity. Further studies of DAMB signaling in <italic>Drosophila</italic>
could have implications for better understanding DA-related neurodegenerative disorders in humans.</p>
</div>
</front>
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<tree><country name="France"><noRegion><name sortKey="Cassar, Marlene" sort="Cassar, Marlene" uniqKey="Cassar M" first="Marlène" last="Cassar">Marlène Cassar</name>
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<name sortKey="Birman, Serge" sort="Birman, Serge" uniqKey="Birman S" first="Serge" last="Birman">Serge Birman</name>
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<name sortKey="Coulom, Helene" sort="Coulom, Helene" uniqKey="Coulom H" first="Hélène" last="Coulom">Hélène Coulom</name>
<name sortKey="Iche Torres, Magali" sort="Iche Torres, Magali" uniqKey="Iche Torres M" first="Magali" last="Iché-Torres">Magali Iché-Torres</name>
<name sortKey="Issa, Abdul Raouf" sort="Issa, Abdul Raouf" uniqKey="Issa A" first="Abdul-Raouf" last="Issa">Abdul-Raouf Issa</name>
<name sortKey="Petitgas, Celine" sort="Petitgas, Celine" uniqKey="Petitgas C" first="Céline" last="Petitgas">Céline Petitgas</name>
<name sortKey="Riemensperger, Thomas" sort="Riemensperger, Thomas" uniqKey="Riemensperger T" first="Thomas" last="Riemensperger">Thomas Riemensperger</name>
<name sortKey="Rival, Thomas" sort="Rival, Thomas" uniqKey="Rival T" first="Thomas" last="Rival">Thomas Rival</name>
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<country name="États-Unis"><noRegion><name sortKey="Han, Kyung An" sort="Han, Kyung An" uniqKey="Han K" first="Kyung-An" last="Han">Kyung-An Han</name>
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