Tyrosine hydroxylase expression and activity in nigrostriatal dopaminergic neurons of MPTP-treated mice at the presymptomatic and symptomatic stages of parkinsonism.
Identifieur interne : 000817 ( Main/Exploration ); précédent : 000816; suivant : 000818Tyrosine hydroxylase expression and activity in nigrostriatal dopaminergic neurons of MPTP-treated mice at the presymptomatic and symptomatic stages of parkinsonism.
Auteurs : Elena A. Kozina [Russie] ; Gulnara R. Khakimova [Russie] ; Vitaly G. Khaindrava [France] ; Valeriayn G. Kucheryanu [Russie] ; Nadezhda E. Vorobyeva [Russie] ; Alexey N. Krasnov [Russie] ; Sophia G. Georgieva [Russie] ; Lidiya Kerkerian-Le Goff [France] ; Michael V. Ugrumov [Russie]Source :
- Journal of the neurological sciences [ 1878-5883 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Aromatic Amino Acid Decarboxylase Inhibitors (pharmacology), Corpus Striatum (pathology), Disease Models, Animal, Dopamine (metabolism), Dopaminergic Neurons (physiology), Electrochemistry, Gene Expression Regulation (drug effects), Hydrazines (pharmacology), Levodopa (metabolism), MPTP Poisoning (pathology), MPTP Poisoning (physiopathology), Male, Mice, Mice, Inbred C57BL, Motor Activity (drug effects), Motor Activity (physiology), RNA, Messenger (metabolism), Substantia Nigra (pathology), Tyrosine 3-Monooxygenase (genetics), Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , genetics : Tyrosine 3-Monooxygenase.
- chemical , metabolism : Dopamine, Levodopa, RNA, Messenger, Tyrosine 3-Monooxygenase.
- chemical , pharmacology : Aromatic Amino Acid Decarboxylase Inhibitors, Hydrazines.
- drug effects : Gene Expression Regulation, Motor Activity.
- pathology : Corpus Striatum, MPTP Poisoning, Substantia Nigra.
- physiology : Dopaminergic Neurons, Motor Activity.
- physiopathology : MPTP Poisoning.
- Animals, Disease Models, Animal, Electrochemistry, Male, Mice, Mice, Inbred C57BL.
Abstract
Progressive degeneration of nigrostriatal dopaminergic (DA-ergic) neurons is a key component in the pathogenesis of Parkinson's disease, which develops for a long time at the preclinical stage with no motor dysfunctions due to the initiation of compensatory processes. The goal of this study was to evaluate the changes in surviving nigrostriatal DA-ergic neurons with focus on tyrosine hydroxylase (TH) in MPTP-treated mice at the presymptomatic and early symptomatic stages of parkinsonism. According to our data, a partial degeneration of DA-ergic neurons at the presymptomatic stage was accompanied by: (i) no change in TH mRNA content in the substantia nigra (SN) suggesting a compensatory increase of TH gene expression in individual neurons; (ii) a decrease of TH protein content in the nigrostriatal system and no change in individual neurons, suggesting a slowdown of TH translation. When comparing DA-ergic neurons at the early symptomatic stage and presymptomatic stage, it becomes evident: (i) a decrease of TH mRNA content in the SN and hence gene expression in individual neurons; (ii) a decrease of TH content in the striatum and its increase in the SN and individual neurons suggesting an acceleration of TH translation. TH activity, an index of the rate of DA synthesis, was unchanged in the SN and decreased in the striatum to the same degree at both stages of parkinsonism. In the meantime, TH activity in individual neurons appeared to be compensatory increased, but to a higher degree at the symptomatic stage than at the presymptomatic one. These data first show that DA depletion, which provokes motor dysfunction, is not a result of the decrease of TH activity and the rate of DA synthesis but is rather related to either a decrease of DA release or an increase of DA uptake in striatal DA-ergic axons.
Url:
DOI: 10.1016/j.jns.2014.03.028
PubMed: 24768159
Affiliations:
- France, Russie
- District fédéral central, Provence-Alpes-Côte d'Azur
- Marseille, Moscou
- Université de la Méditerranée
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Le document en format XML
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Khaindrava</name><affiliation wicri:level="4"><nlm:affiliation>Laboratory of Neurohistology, Institute of Normal Physiology RAMS, Moscow, Russia; IC2N, IBDML, UMR6216 CNRS-Université de la Méditerranée, Marseille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Laboratory of Neurohistology, Institute of Normal Physiology RAMS, Moscow, Russia; IC2N, IBDML, UMR6216 CNRS-Université de la Méditerranée, Marseille</wicri:regionArea><placeName><region type="region">Provence-Alpes-Côte d'Azur</region><region type="old region">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université de la Méditerranée</orgName></affiliation></author><author><name sortKey="Kucheryanu, Valeriayn G" sort="Kucheryanu, Valeriayn G" uniqKey="Kucheryanu V" first="Valeriayn G" last="Kucheryanu">Valeriayn G. Kucheryanu</name><affiliation wicri:level="3"><nlm:affiliation>Laboratory of General Pathophysiology of Nervous System, Institute of General Pathology and Pathological Physiology, RAMS, Moscow, Russia.</nlm:affiliation><country xml:lang="fr">Russie</country><wicri:regionArea>Laboratory of General Pathophysiology of Nervous System, Institute of General Pathology and Pathological Physiology, RAMS, Moscow</wicri:regionArea><placeName><settlement type="city">Moscou</settlement><region>District fédéral central</region></placeName></affiliation></author><author><name sortKey="Vorobyeva, Nadezhda E" sort="Vorobyeva, Nadezhda E" uniqKey="Vorobyeva N" first="Nadezhda E" last="Vorobyeva">Nadezhda E. 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Krasnov</name><affiliation wicri:level="3"><nlm:affiliation>Laboratory of Gene Expression Regulation, Institute of Gene Biology RAS, Moscow, Russia.</nlm:affiliation><country xml:lang="fr">Russie</country><wicri:regionArea>Laboratory of Gene Expression Regulation, Institute of Gene Biology RAS, Moscow</wicri:regionArea><placeName><settlement type="city">Moscou</settlement><region>District fédéral central</region></placeName></affiliation></author><author><name sortKey="Georgieva, Sophia G" sort="Georgieva, Sophia G" uniqKey="Georgieva S" first="Sophia G" last="Georgieva">Sophia G. Georgieva</name><affiliation wicri:level="3"><nlm:affiliation>Laboratory of Gene Expression Regulation, Institute of Gene Biology RAS, Moscow, Russia.</nlm:affiliation><country xml:lang="fr">Russie</country><wicri:regionArea>Laboratory of Gene Expression Regulation, Institute of Gene Biology RAS, Moscow</wicri:regionArea><placeName><settlement type="city">Moscou</settlement><region>District fédéral central</region></placeName></affiliation></author><author><name sortKey="Kerkerian Le Goff, Lidiya" sort="Kerkerian Le Goff, Lidiya" uniqKey="Kerkerian Le Goff L" first="Lidiya" last="Kerkerian-Le Goff">Lidiya Kerkerian-Le Goff</name><affiliation wicri:level="4"><nlm:affiliation>IC2N, IBDML, UMR6216 CNRS-Université de la Méditerranée, Marseille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>IC2N, IBDML, UMR6216 CNRS-Université de la Méditerranée, Marseille</wicri:regionArea><placeName><region type="region">Provence-Alpes-Côte d'Azur</region><region type="old region">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName><orgName type="university">Université de la Méditerranée</orgName></affiliation></author><author><name sortKey="Ugrumov, Michael V" sort="Ugrumov, Michael V" uniqKey="Ugrumov M" first="Michael V" last="Ugrumov">Michael V. Ugrumov</name><affiliation wicri:level="3"><nlm:affiliation>Laboratory of Hormonal Regulations, Institute of Developmental Biology RAS, Moscow, Russia; Laboratory of Neurohistology, Institute of Normal Physiology RAMS, Moscow, Russia. Electronic address: michael.ugrumov@mail.ru.</nlm:affiliation><country xml:lang="fr">Russie</country><wicri:regionArea>Laboratory of Hormonal Regulations, Institute of Developmental Biology RAS, Moscow, Russia; Laboratory of Neurohistology, Institute of Normal Physiology RAMS, Moscow</wicri:regionArea><placeName><settlement type="city">Moscou</settlement><region>District fédéral central</region></placeName></affiliation></author></analytic><series><title level="j">Journal of the neurological sciences</title><idno type="eISSN">1878-5883</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Aromatic Amino Acid Decarboxylase Inhibitors (pharmacology)</term><term>Corpus Striatum (pathology)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Dopaminergic Neurons (physiology)</term><term>Electrochemistry</term><term>Gene Expression Regulation (drug effects)</term><term>Hydrazines (pharmacology)</term><term>Levodopa (metabolism)</term><term>MPTP Poisoning (pathology)</term><term>MPTP Poisoning (physiopathology)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Motor Activity (drug effects)</term><term>Motor Activity (physiology)</term><term>RNA, Messenger (metabolism)</term><term>Substantia Nigra (pathology)</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>Dopamine</term><term>Levodopa</term><term>RNA, Messenger</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Aromatic Amino Acid Decarboxylase Inhibitors</term><term>Hydrazines</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation</term><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>MPTP Poisoning</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Dopaminergic Neurons</term><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>MPTP Poisoning</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Electrochemistry</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Progressive degeneration of nigrostriatal dopaminergic (DA-ergic) neurons is a key component in the pathogenesis of Parkinson's disease, which develops for a long time at the preclinical stage with no motor dysfunctions due to the initiation of compensatory processes. The goal of this study was to evaluate the changes in surviving nigrostriatal DA-ergic neurons with focus on tyrosine hydroxylase (TH) in MPTP-treated mice at the presymptomatic and early symptomatic stages of parkinsonism. According to our data, a partial degeneration of DA-ergic neurons at the presymptomatic stage was accompanied by: (i) no change in TH mRNA content in the substantia nigra (SN) suggesting a compensatory increase of TH gene expression in individual neurons; (ii) a decrease of TH protein content in the nigrostriatal system and no change in individual neurons, suggesting a slowdown of TH translation. When comparing DA-ergic neurons at the early symptomatic stage and presymptomatic stage, it becomes evident: (i) a decrease of TH mRNA content in the SN and hence gene expression in individual neurons; (ii) a decrease of TH content in the striatum and its increase in the SN and individual neurons suggesting an acceleration of TH translation. TH activity, an index of the rate of DA synthesis, was unchanged in the SN and decreased in the striatum to the same degree at both stages of parkinsonism. In the meantime, TH activity in individual neurons appeared to be compensatory increased, but to a higher degree at the symptomatic stage than at the presymptomatic one. These data first show that DA depletion, which provokes motor dysfunction, is not a result of the decrease of TH activity and the rate of DA synthesis but is rather related to either a decrease of DA release or an increase of DA uptake in striatal DA-ergic axons.</div></front></TEI><affiliations><list><country><li>France</li><li>Russie</li></country><region><li>District fédéral central</li><li>Provence-Alpes-Côte d'Azur</li></region><settlement><li>Marseille</li><li>Moscou</li></settlement><orgName><li>Université de la Méditerranée</li></orgName></list><tree><country name="Russie"><region name="District fédéral central"><name sortKey="Kozina, Elena A" sort="Kozina, Elena A" uniqKey="Kozina E" first="Elena A" last="Kozina">Elena A. Kozina</name></region><name sortKey="Georgieva, Sophia G" sort="Georgieva, Sophia G" uniqKey="Georgieva S" first="Sophia G" last="Georgieva">Sophia G. Georgieva</name><name sortKey="Khakimova, Gulnara R" sort="Khakimova, Gulnara R" uniqKey="Khakimova G" first="Gulnara R" last="Khakimova">Gulnara R. Khakimova</name><name sortKey="Krasnov, Alexey N" sort="Krasnov, Alexey N" uniqKey="Krasnov A" first="Alexey N" last="Krasnov">Alexey N. Krasnov</name><name sortKey="Kucheryanu, Valeriayn G" sort="Kucheryanu, Valeriayn G" uniqKey="Kucheryanu V" first="Valeriayn G" last="Kucheryanu">Valeriayn G. Kucheryanu</name><name sortKey="Ugrumov, Michael V" sort="Ugrumov, Michael V" uniqKey="Ugrumov M" first="Michael V" last="Ugrumov">Michael V. Ugrumov</name><name sortKey="Vorobyeva, Nadezhda E" sort="Vorobyeva, Nadezhda E" uniqKey="Vorobyeva N" first="Nadezhda E" last="Vorobyeva">Nadezhda E. Vorobyeva</name></country><country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Khaindrava, Vitaly G" sort="Khaindrava, Vitaly G" uniqKey="Khaindrava V" first="Vitaly G" last="Khaindrava">Vitaly G. Khaindrava</name></region><name sortKey="Kerkerian Le Goff, Lidiya" sort="Kerkerian Le Goff, Lidiya" uniqKey="Kerkerian Le Goff L" first="Lidiya" last="Kerkerian-Le Goff">Lidiya Kerkerian-Le Goff</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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