Effect of serotonin transporter blockade on L-DOPA-induced dyskinesia in animal models of Parkinson's disease.
Identifieur interne : 001690 ( Ncbi/Curation ); précédent : 001689; suivant : 001691Effect of serotonin transporter blockade on L-DOPA-induced dyskinesia in animal models of Parkinson's disease.
Auteurs : C. Fidalgo [Italie] ; W K D. Ko [Royaume-Uni] ; E. Tronci [Italie] ; Q. Li [République populaire de Chine] ; R. Stancampiano [Italie] ; Q. Chuan [République populaire de Chine] ; E. Bezard [République populaire de Chine] ; M. Carta [Italie]Source :
- Neuroscience [ 1873-7544 ] ; 2015.
English descriptors
- KwdEn :
- Analysis of Variance, Animals, Antiparkinson Agents (adverse effects), Citalopram (therapeutic use), Disease Models, Animal, Dyskinesia, Drug-Induced (drug therapy), Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (metabolism), Female, Levodopa (adverse effects), MPTP Poisoning (chemically induced), MPTP Poisoning (drug therapy), Macaca fascicularis, Male, Oxidopamine (toxicity), Parkinson Disease (drug therapy), Parkinson Disease (etiology), Rats, Rats, Sprague-Dawley, Serotonin Plasma Membrane Transport Proteins (metabolism), Serotonin Uptake Inhibitors (therapeutic use), Time Factors, Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , metabolism : Serotonin Plasma Membrane Transport Proteins, Tyrosine 3-Monooxygenase.
- chemical , therapeutic use : Citalopram, Serotonin Uptake Inhibitors.
- chemically induced : MPTP Poisoning.
- drug therapy : Dyskinesia, Drug-Induced, MPTP Poisoning, Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced, Parkinson Disease.
- metabolism : Dyskinesia, Drug-Induced.
- chemical , toxicity : Oxidopamine.
- Analysis of Variance, Animals, Disease Models, Animal, Female, Macaca fascicularis, Male, Rats, Rats, Sprague-Dawley, Time Factors.
Abstract
Serotonin transporter blockade with selective serotonin reuptake inhibitors (SSRIs) was recently shown to counteract L-DOPA-induced dyskinesia in 6-hydroxydopamine (6-OHDA)-lesioned rats. However, this effect has never been described in Parkinson's disease (PD) patients, despite that they often receive SSRIs for the treatment of depression. In the present study, we investigated the efficacy of the SSRI citalopram against dyskinesia in two experimental models of PD, the 6-OHDA-lesioned rat and 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine (MPTP)-treated macaque. First, we studied the acute and chronic effect of citalopram, given at different time points before L-DOPA, in L-DOPA-primed parkinsonian rats. Moreover, the acute effect of citalopram was also evaluated in dyskinetic MPTP-treated macaques. In L-DOPA-primed rats, a significant and long-lasting reduction of L-DOPA-induced dyskinesia (LID) was observed only when citalopram was given 30 min before L-DOPA, suggesting that the time of injection relative to L-DOPA is a key factor for the efficacy of the treatment. Interestingly, an acute challenge with the 5-HT1A/1B receptor agonist eltoprazine, given at the end of the chronic study, was equally effective in reducing LID in rats previously chronically treated with L-DOPA or L-DOPA plus citalopram, suggesting that no auto-receptor desensitization was induced by chronic citalopram treatment. In MPTP-treated macaques, citalopram produced a striking suppression of LID but at the expense of L-DOPA therapeutic efficacy, which represents a concern for possible clinical application.
DOI: 10.1016/j.neuroscience.2015.04.027
PubMed: 25907446
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Chuan</name><affiliation wicri:level="3"><nlm:affiliation>Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Bezard, E" sort="Bezard, E" uniqKey="Bezard E" first="E" last="Bezard">E. Bezard</name><affiliation wicri:level="3"><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Motac Neuroscience, Manchester, UK; Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Motac Neuroscience, Manchester, UK; Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Carta, M" sort="Carta, M" uniqKey="Carta M" first="M" last="Carta">M. Carta</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Sciences, Section of Physiology, University of Cagliari, University Campus, SS554 km 4.5, 09042 Monserrato, Italy. 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Fidalgo</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Sciences, Section of Physiology, University of Cagliari, University Campus, SS554 km 4.5, 09042 Monserrato, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Biomedical Sciences, Section of Physiology, University of Cagliari, University Campus, SS554 km 4.5, 09042 Monserrato</wicri:regionArea><wicri:noRegion>09042 Monserrato</wicri:noRegion></affiliation></author><author><name sortKey="Ko, W K D" sort="Ko, W K D" uniqKey="Ko W" first="W K D" last="Ko">W K D. Ko</name><affiliation wicri:level="3"><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Motac Neuroscience, Manchester, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Motac Neuroscience, Manchester</wicri:regionArea><placeName><settlement type="city">Manchester</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Manchester</region></placeName></affiliation></author><author><name sortKey="Tronci, E" sort="Tronci, E" uniqKey="Tronci E" first="E" last="Tronci">E. Tronci</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Sciences, Section of Physiology, University of Cagliari, University Campus, SS554 km 4.5, 09042 Monserrato, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Biomedical Sciences, Section of Physiology, University of Cagliari, University Campus, SS554 km 4.5, 09042 Monserrato</wicri:regionArea><wicri:noRegion>09042 Monserrato</wicri:noRegion></affiliation></author><author><name sortKey="Li, Q" sort="Li, Q" uniqKey="Li Q" first="Q" last="Li">Q. Li</name><affiliation wicri:level="3"><nlm:affiliation>Motac Neuroscience, Manchester, UK; Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Motac Neuroscience, Manchester, UK; Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Stancampiano, R" sort="Stancampiano, R" uniqKey="Stancampiano R" first="R" last="Stancampiano">R. Stancampiano</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Sciences, Section of Physiology, University of Cagliari, University Campus, SS554 km 4.5, 09042 Monserrato, Italy.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Biomedical Sciences, Section of Physiology, University of Cagliari, University Campus, SS554 km 4.5, 09042 Monserrato</wicri:regionArea><wicri:noRegion>09042 Monserrato</wicri:noRegion></affiliation></author><author><name sortKey="Chuan, Q" sort="Chuan, Q" uniqKey="Chuan Q" first="Q" last="Chuan">Q. Chuan</name><affiliation wicri:level="3"><nlm:affiliation>Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Bezard, E" sort="Bezard, E" uniqKey="Bezard E" first="E" last="Bezard">E. Bezard</name><affiliation wicri:level="3"><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Motac Neuroscience, Manchester, UK; Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Motac Neuroscience, Manchester, UK; Institute of Lab Animal Sciences, China Academy of Medical Sciences, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Carta, M" sort="Carta, M" uniqKey="Carta M" first="M" last="Carta">M. Carta</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biomedical Sciences, Section of Physiology, University of Cagliari, University Campus, SS554 km 4.5, 09042 Monserrato, Italy. Electronic address: manolocarta@unica.it.</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Biomedical Sciences, Section of Physiology, University of Cagliari, University Campus, SS554 km 4.5, 09042 Monserrato</wicri:regionArea><wicri:noRegion>09042 Monserrato</wicri:noRegion></affiliation></author></analytic><series><title level="j">Neuroscience</title><idno type="eISSN">1873-7544</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Antiparkinson Agents (adverse effects)</term><term>Citalopram (therapeutic use)</term><term>Disease Models, Animal</term><term>Dyskinesia, Drug-Induced (drug therapy)</term><term>Dyskinesia, Drug-Induced (etiology)</term><term>Dyskinesia, Drug-Induced (metabolism)</term><term>Female</term><term>Levodopa (adverse effects)</term><term>MPTP Poisoning (chemically induced)</term><term>MPTP Poisoning (drug therapy)</term><term>Macaca fascicularis</term><term>Male</term><term>Oxidopamine (toxicity)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (etiology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Serotonin Plasma Membrane Transport Proteins (metabolism)</term><term>Serotonin Uptake Inhibitors (therapeutic use)</term><term>Time Factors</term><term>Tyrosine 3-Monooxygenase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Serotonin Plasma Membrane Transport Proteins</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Citalopram</term><term>Serotonin Uptake Inhibitors</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>MPTP Poisoning</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>MPTP Poisoning</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Oxidopamine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Macaca fascicularis</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Serotonin transporter blockade with selective serotonin reuptake inhibitors (SSRIs) was recently shown to counteract L-DOPA-induced dyskinesia in 6-hydroxydopamine (6-OHDA)-lesioned rats. However, this effect has never been described in Parkinson's disease (PD) patients, despite that they often receive SSRIs for the treatment of depression. In the present study, we investigated the efficacy of the SSRI citalopram against dyskinesia in two experimental models of PD, the 6-OHDA-lesioned rat and 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine (MPTP)-treated macaque. First, we studied the acute and chronic effect of citalopram, given at different time points before L-DOPA, in L-DOPA-primed parkinsonian rats. Moreover, the acute effect of citalopram was also evaluated in dyskinetic MPTP-treated macaques. In L-DOPA-primed rats, a significant and long-lasting reduction of L-DOPA-induced dyskinesia (LID) was observed only when citalopram was given 30 min before L-DOPA, suggesting that the time of injection relative to L-DOPA is a key factor for the efficacy of the treatment. Interestingly, an acute challenge with the 5-HT1A/1B receptor agonist eltoprazine, given at the end of the chronic study, was equally effective in reducing LID in rats previously chronically treated with L-DOPA or L-DOPA plus citalopram, suggesting that no auto-receptor desensitization was induced by chronic citalopram treatment. In MPTP-treated macaques, citalopram produced a striking suppression of LID but at the expense of L-DOPA therapeutic efficacy, which represents a concern for possible clinical application.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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