Progressive Parkinsonism by acute dysfunction of excitatory amino acid transporters in the rat substantia nigra.
Identifieur interne : 001318 ( Ncbi/Curation ); précédent : 001317; suivant : 001319Progressive Parkinsonism by acute dysfunction of excitatory amino acid transporters in the rat substantia nigra.
Auteurs : Maxime Assous [France] ; Laurence Had-Aissouni [France] ; Paolo Gubellini [France] ; Christophe Melon [France] ; Imane Nafia [France] ; Pascal Salin [France] ; Lydia Kerkerian-Le-Goff [France] ; Philippe Kachidian [France]Source :
- Neurobiology of disease [ 1095-953X ] ; 2014.
English descriptors
- KwdEn :
- Acetylcysteine (therapeutic use), Action Potentials (drug effects), Animals, Dicarboxylic Acids (toxicity), Disease Models, Animal, Exploratory Behavior (physiology), Forelimb (physiopathology), Free Radical Scavengers (therapeutic use), Functional Laterality, Glutamate Decarboxylase (metabolism), Glutamate Plasma Membrane Transport Proteins (metabolism), In Vitro Techniques, Male, Motor Activity (drug effects), Neuroglia (pathology), Neurotransmitter Uptake Inhibitors (toxicity), Parkinsonian Disorders (chemically induced), Parkinsonian Disorders (drug therapy), Parkinsonian Disorders (metabolism), Parkinsonian Disorders (pathology), Pyrrolidines (toxicity), Rats, Rats, Wistar, Substantia Nigra (drug effects), Substantia Nigra (metabolism), Thiobarbituric Acid Reactive Substances (metabolism), Tyrosine 3-Monooxygenase (genetics), Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , genetics : Tyrosine 3-Monooxygenase.
- chemical , metabolism : Glutamate Decarboxylase, Glutamate Plasma Membrane Transport Proteins, Thiobarbituric Acid Reactive Substances, Tyrosine 3-Monooxygenase.
- chemical , therapeutic use : Acetylcysteine, Free Radical Scavengers.
- chemically induced : Parkinsonian Disorders.
- drug effects : Action Potentials, Motor Activity, Substantia Nigra.
- drug therapy : Parkinsonian Disorders.
- metabolism : Parkinsonian Disorders, Substantia Nigra.
- pathology : Neuroglia, Parkinsonian Disorders.
- physiology : Exploratory Behavior.
- physiopathology : Forelimb.
- chemical , toxicity : Dicarboxylic Acids, Neurotransmitter Uptake Inhibitors, Pyrrolidines.
- Animals, Disease Models, Animal, Functional Laterality, In Vitro Techniques, Male, Rats, Rats, Wistar.
Abstract
Parkinson's disease (PD) is characterized by the progressive degeneration of substantia nigra (SN) dopamine neurons, involving a multifactorial cascade of pathogenic events. Here we explored the hypothesis that dysfunction of excitatory amino acid transporters (EAATs) might be involved. Acutely-induced dysfunction of EAATs in the rat SN, by single unilateral injection of their substrate inhibitor l-trans-pyrrolidine-2,4-dicarboxylate (PDC), triggers a neurodegenerative process mimicking several PD features. Dopamine neurons are selectively affected, consistent with their sustained excitation by PDC measured by slice electrophysiology. The anti-oxidant N-acetylcysteine and the NMDA receptor antagonists ifenprodil and memantine provide neuroprotection. Besides oxidative stress and NMDA receptor-mediated excitotoxicity, glutathione depletion and neuroinflammation characterize the primary insult. Most interestingly, the degeneration progresses overtime with unilateral to bilateral and caudo-rostral evolution. Transient adaptive changes in dopamine function markers in SN and striatum accompany cell loss and axonal dystrophy, respectively. Motor deficits appear when neuron loss exceeds 50% in the most affected SN and striatal dopamine tone is dramatically reduced. These findings outline a functional link between EAAT dysfunction and several PD pathogenic mechanisms/pathological hallmarks, and provide a novel acutely-triggered model of progressive Parkinsonism.
DOI: 10.1016/j.nbd.2014.01.011
PubMed: 24480091
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Electronic address: lydia.kerkerian-le-goff@univ-amu.fr.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille</wicri:regionArea><placeName><region type="region" nuts="2">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université d'Aix-Marseille</orgName></affiliation></author><author><name sortKey="Kachidian, Philippe" sort="Kachidian, Philippe" uniqKey="Kachidian P" first="Philippe" last="Kachidian">Philippe Kachidian</name><affiliation wicri:level="4"><nlm:affiliation>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille, France. Electronic address: philippe.kachidian@univ-amu.fr.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille</wicri:regionArea><placeName><region type="region" nuts="2">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université d'Aix-Marseille</orgName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24480091</idno><idno type="pmid">24480091</idno><idno type="doi">10.1016/j.nbd.2014.01.011</idno><idno type="wicri:Area/PubMed/Corpus">000572</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000572</idno><idno type="wicri:Area/PubMed/Curation">000554</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000554</idno><idno 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d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université d'Aix-Marseille</orgName></affiliation></author><author><name sortKey="Had Aissouni, Laurence" sort="Had Aissouni, Laurence" uniqKey="Had Aissouni L" first="Laurence" last="Had-Aissouni">Laurence Had-Aissouni</name><affiliation wicri:level="4"><nlm:affiliation>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille</wicri:regionArea><placeName><region type="region" nuts="2">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université d'Aix-Marseille</orgName></affiliation></author><author><name sortKey="Gubellini, Paolo" sort="Gubellini, Paolo" uniqKey="Gubellini P" first="Paolo" last="Gubellini">Paolo Gubellini</name><affiliation wicri:level="4"><nlm:affiliation>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille</wicri:regionArea><placeName><region type="region" nuts="2">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université d'Aix-Marseille</orgName></affiliation></author><author><name sortKey="Melon, Christophe" sort="Melon, Christophe" uniqKey="Melon C" first="Christophe" last="Melon">Christophe Melon</name><affiliation wicri:level="4"><nlm:affiliation>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille</wicri:regionArea><placeName><region type="region" nuts="2">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université d'Aix-Marseille</orgName></affiliation></author><author><name sortKey="Nafia, Imane" sort="Nafia, Imane" uniqKey="Nafia I" first="Imane" last="Nafia">Imane Nafia</name><affiliation wicri:level="3"><nlm:affiliation>Fluofarma, 2 Rue Robert Escarpit, 33607, Pessac, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Fluofarma, 2 Rue Robert Escarpit, 33607, Pessac</wicri:regionArea><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Pessac</settlement></placeName></affiliation></author><author><name sortKey="Salin, Pascal" sort="Salin, Pascal" uniqKey="Salin P" first="Pascal" last="Salin">Pascal Salin</name><affiliation wicri:level="4"><nlm:affiliation>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille</wicri:regionArea><placeName><region type="region" nuts="2">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université d'Aix-Marseille</orgName></affiliation></author><author><name sortKey="Kerkerian Le Goff, Lydia" sort="Kerkerian Le Goff, Lydia" uniqKey="Kerkerian Le Goff L" first="Lydia" last="Kerkerian-Le-Goff">Lydia Kerkerian-Le-Goff</name><affiliation wicri:level="4"><nlm:affiliation>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille, France. Electronic address: lydia.kerkerian-le-goff@univ-amu.fr.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille</wicri:regionArea><placeName><region type="region" nuts="2">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université d'Aix-Marseille</orgName></affiliation></author><author><name sortKey="Kachidian, Philippe" sort="Kachidian, Philippe" uniqKey="Kachidian P" first="Philippe" last="Kachidian">Philippe Kachidian</name><affiliation wicri:level="4"><nlm:affiliation>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille, France. Electronic address: philippe.kachidian@univ-amu.fr.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Aix-Marseille Université, CNRS, IBDML, UMR7288, 13009, Case 907, Parc Scientifique de Luminy, 13009 Marseille</wicri:regionArea><placeName><region type="region" nuts="2">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université d'Aix-Marseille</orgName></affiliation></author></analytic><series><title level="j">Neurobiology of disease</title><idno type="eISSN">1095-953X</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylcysteine (therapeutic use)</term><term>Action Potentials (drug effects)</term><term>Animals</term><term>Dicarboxylic Acids (toxicity)</term><term>Disease Models, Animal</term><term>Exploratory Behavior (physiology)</term><term>Forelimb (physiopathology)</term><term>Free Radical Scavengers (therapeutic use)</term><term>Functional Laterality</term><term>Glutamate Decarboxylase (metabolism)</term><term>Glutamate Plasma Membrane Transport Proteins (metabolism)</term><term>In Vitro Techniques</term><term>Male</term><term>Motor Activity (drug effects)</term><term>Neuroglia (pathology)</term><term>Neurotransmitter Uptake Inhibitors (toxicity)</term><term>Parkinsonian Disorders (chemically induced)</term><term>Parkinsonian Disorders (drug therapy)</term><term>Parkinsonian Disorders (metabolism)</term><term>Parkinsonian Disorders (pathology)</term><term>Pyrrolidines (toxicity)</term><term>Rats</term><term>Rats, Wistar</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (metabolism)</term><term>Thiobarbituric Acid Reactive Substances (metabolism)</term><term>Tyrosine 3-Monooxygenase (genetics)</term><term>Tyrosine 3-Monooxygenase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutamate Decarboxylase</term><term>Glutamate Plasma Membrane Transport Proteins</term><term>Thiobarbituric Acid Reactive Substances</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Acetylcysteine</term><term>Free Radical Scavengers</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Action Potentials</term><term>Motor Activity</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinsonian Disorders</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neuroglia</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Exploratory Behavior</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Forelimb</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Dicarboxylic Acids</term><term>Neurotransmitter Uptake Inhibitors</term><term>Pyrrolidines</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Functional Laterality</term><term>In Vitro Techniques</term><term>Male</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is characterized by the progressive degeneration of substantia nigra (SN) dopamine neurons, involving a multifactorial cascade of pathogenic events. Here we explored the hypothesis that dysfunction of excitatory amino acid transporters (EAATs) might be involved. Acutely-induced dysfunction of EAATs in the rat SN, by single unilateral injection of their substrate inhibitor l-trans-pyrrolidine-2,4-dicarboxylate (PDC), triggers a neurodegenerative process mimicking several PD features. Dopamine neurons are selectively affected, consistent with their sustained excitation by PDC measured by slice electrophysiology. The anti-oxidant N-acetylcysteine and the NMDA receptor antagonists ifenprodil and memantine provide neuroprotection. Besides oxidative stress and NMDA receptor-mediated excitotoxicity, glutathione depletion and neuroinflammation characterize the primary insult. Most interestingly, the degeneration progresses overtime with unilateral to bilateral and caudo-rostral evolution. Transient adaptive changes in dopamine function markers in SN and striatum accompany cell loss and axonal dystrophy, respectively. Motor deficits appear when neuron loss exceeds 50% in the most affected SN and striatal dopamine tone is dramatically reduced. These findings outline a functional link between EAAT dysfunction and several PD pathogenic mechanisms/pathological hallmarks, and provide a novel acutely-triggered model of progressive Parkinsonism.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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