Effects of riluzole on the electrophysiological activity of pallidal neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkey
Identifieur interne : 003A44 ( Main/Exploration ); précédent : 003A43; suivant : 003A45Effects of riluzole on the electrophysiological activity of pallidal neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkey
Auteurs : Th Boraud [France] ; E. Bezard [France] ; J. M Stutzmann [France] ; B. Bioulac [France] ; C. E Gross [France]Source :
- Neuroscience Letters [ 0304-3940 ] ; 2000.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animal model, Animals, Antiparkinson Agents (pharmacology), Antiparkinson agent, Chemotherapy, Comparative study, Dopamine Agents, Dyskinesia, Electrophysiology, Female, Globus Pallidus (cytology), Globus Pallidus (drug effects), Globus Pallidus (physiology), Globus pallidus, Levodopa, Levodopa (pharmacology), Macaca mulatta, Monkey, Neurons (drug effects), Neurons (physiology), Neuroprotective Agents (pharmacology), Pallidum, Parkinson Disease, Secondary (etiology), Parkinson Disease, Secondary (physiopathology), Parkinson disease, Parkinson’s disease, Riluzole, Riluzole (pharmacology), Single unit recordings, Treatment, Unit response.
- MESH :
- chemical , pharmacology : Antiparkinson Agents, Levodopa, Neuroprotective Agents, Riluzole.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents.
- cytology : Globus Pallidus.
- drug effects : Globus Pallidus, Neurons.
- etiology : Parkinson Disease, Secondary.
- physiology : Globus Pallidus, Neurons.
- physiopathology : Parkinson Disease, Secondary.
- Animals, Electrophysiology, Female, Macaca mulatta.
Abstract
The effect of riluzole administration, an antiglutamatergic compound, on the electrophysiological activity of the pallidal complex of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys is compared with those induced by two dosages of levodopa (l-DOPA), the first affording the best clinical alleviation, the second sufficient to induce dyskinesias. Both dosages of l-DOPA reduced sharply the firing frequency of globus pallidus pars internalis (GPi) neurons (respectively, 43.8±23.0 and 27.4±20.2 vs. 111.2±31.4 Hz), decreased the percentage of bursting cells (respectively, 60.7 and 50.0 vs. 80.3%) and augmented the number of regular cells (respectively, 6.5 and 33.0 vs. 4.8%). Riluzole restored the firing frequency (75.0±26.9 Hz) and the firing pattern of the GPi (39.7% bursting, 9.5% regular and 50.8% irregular). These results suggest that the emergence of dyskinesia may well be due to a modification of the neuronal messages transmitted from the GPi to the motor nuclei of the thalamus. Riluzole would represent an interesting alternative to dopamine therapy in Parkinson's disease since it regularizes firing but does not cause dyskinesia.
Url:
DOI: 10.1016/S0304-3940(00)00780-1
Affiliations:
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M Stutzmann</name><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Rhône Poulenc Rorer SA, Département de Biologie, Centre de Recherche de Vitry Alfortville, 13 quai Jules Guesde, 94403 Vitry sur Seine</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Vitry sur Seine</settlement></placeName></affiliation></author><author><name sortKey="Bioulac, B" sort="Bioulac, B" uniqKey="Bioulac B" first="B" last="Bioulac">B. 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E Gross</name><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Basal Gang, CNRS UMR 5543, Université Victor Segalen-Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux Cedex</wicri:regionArea><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Bordeaux</settlement></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Neuroscience Letters</title><title level="j" type="abbrev">NSL</title><idno type="ISSN">0304-3940</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">281</biblScope><biblScope unit="issue">2–3</biblScope><biblScope unit="page" from="75">75</biblScope><biblScope unit="page" to="78">78</biblScope></imprint><idno type="ISSN">0304-3940</idno></series><idno type="istex">2B6B3B5D45BDB68C80A119BB48A11713CAB0156D</idno><idno type="DOI">10.1016/S0304-3940(00)00780-1</idno><idno type="PII">S0304-3940(00)00780-1</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0304-3940</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Animal model</term><term>Animals</term><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson agent</term><term>Chemotherapy</term><term>Comparative study</term><term>Dopamine Agents</term><term>Dyskinesia</term><term>Electrophysiology</term><term>Female</term><term>Globus Pallidus (cytology)</term><term>Globus Pallidus (drug effects)</term><term>Globus Pallidus (physiology)</term><term>Globus pallidus</term><term>Levodopa</term><term>Levodopa (pharmacology)</term><term>Macaca mulatta</term><term>Monkey</term><term>Neurons (drug effects)</term><term>Neurons (physiology)</term><term>Neuroprotective Agents (pharmacology)</term><term>Pallidum</term><term>Parkinson Disease, Secondary (etiology)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Parkinson disease</term><term>Parkinson’s disease</term><term>Riluzole</term><term>Riluzole (pharmacology)</term><term>Single unit recordings</term><term>Treatment</term><term>Unit response</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term><term>Neuroprotective Agents</term><term>Riluzole</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Dopamine Agents</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Globus Pallidus</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Globus Pallidus</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Globus Pallidus</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Electrophysiology</term><term>Female</term><term>Macaca mulatta</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Antiparkinsonien</term><term>Chimiothérapie</term><term>Dyskinésie</term><term>Décharge unitaire</term><term>Etude comparative</term><term>Lévodopa</term><term>MPTP</term><term>Modèle animal</term><term>Pallidum</term><term>Parkinson maladie</term><term>Riluzole</term><term>Singe</term><term>Traitement</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The effect of riluzole administration, an antiglutamatergic compound, on the electrophysiological activity of the pallidal complex of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys is compared with those induced by two dosages of levodopa (l-DOPA), the first affording the best clinical alleviation, the second sufficient to induce dyskinesias. Both dosages of l-DOPA reduced sharply the firing frequency of globus pallidus pars internalis (GPi) neurons (respectively, 43.8±23.0 and 27.4±20.2 vs. 111.2±31.4 Hz), decreased the percentage of bursting cells (respectively, 60.7 and 50.0 vs. 80.3%) and augmented the number of regular cells (respectively, 6.5 and 33.0 vs. 4.8%). Riluzole restored the firing frequency (75.0±26.9 Hz) and the firing pattern of the GPi (39.7% bursting, 9.5% regular and 50.8% irregular). These results suggest that the emergence of dyskinesia may well be due to a modification of the neuronal messages transmitted from the GPi to the motor nuclei of the thalamus. Riluzole would represent an interesting alternative to dopamine therapy in Parkinson's disease since it regularizes firing but does not cause dyskinesia.</div></front></TEI><affiliations><list><country><li>France</li></country><region><li>Aquitaine</li><li>Nouvelle-Aquitaine</li><li>Île-de-France</li></region><settlement><li>Bordeaux</li><li>Vitry sur Seine</li></settlement></list><tree><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Boraud, Th" sort="Boraud, Th" uniqKey="Boraud T" first="Th" last="Boraud">Th Boraud</name></region><name sortKey="Bezard, E" sort="Bezard, E" uniqKey="Bezard E" first="E" last="Bezard">E. Bezard</name><name sortKey="Bioulac, B" sort="Bioulac, B" uniqKey="Bioulac B" first="B" last="Bioulac">B. Bioulac</name><name sortKey="Boraud, Th" sort="Boraud, Th" uniqKey="Boraud T" first="Th" last="Boraud">Th Boraud</name><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C. E" last="Gross">C. E Gross</name><name sortKey="Stutzmann, J M" sort="Stutzmann, J M" uniqKey="Stutzmann J" first="J. M" last="Stutzmann">J. M Stutzmann</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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