Effects of CB1 cannabinoid receptor modulating compounds on the hyperkinesia induced by high‐dose levodopa in the reserpine‐treated rat model of Parkinson's disease
Identifieur interne : 004107 ( Main/Exploration ); précédent : 004106; suivant : 004108Effects of CB1 cannabinoid receptor modulating compounds on the hyperkinesia induced by high‐dose levodopa in the reserpine‐treated rat model of Parkinson's disease
Auteurs : Gregorio Segovia [Royaume-Uni, Espagne] ; Francisco Mora [Espagne] ; Alan R. Crossman [Royaume-Uni] ; Jonathan M. Brotchie [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2003-02.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adrenergic Uptake Inhibitors (therapeutic use), Alkaloid, Animal, Animal model, Animals, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (adverse effects), Antiparkinson agent, Behavior, Animal (drug effects), CB1 cannabinoid receptor, CB1 receptors, Cannabinoid Receptor Modulators, Disease Models, Animal, Dose-Response Relationship, Drug, Fatty Acids, Unsaturated (pharmacology), Hyperkinesia, Hyperkinesis (chemically induced), Levodopa, Levodopa (administration & dosage), Levodopa (adverse effects), L‐dopa, Male, Parkinson Disease (drug therapy), Parkinson disease, Pathophysiology, Rat, Rats, Rats, Sprague-Dawley, Receptors, Cannabinoid, Receptors, Drug (drug effects), Reserpine, Reserpine (therapeutic use), Time Factors, cannabinoids, dyskinesia, reserpine.
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Levodopa.
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , drug effects : Receptors, Drug.
- chemical , pharmacology : Fatty Acids, Unsaturated.
- chemical , therapeutic use : Adrenergic Uptake Inhibitors, Reserpine.
- chemically induced : Hyperkinesis.
- drug effects : Behavior, Animal.
- drug therapy : Parkinson Disease.
- Animals, Cannabinoid Receptor Modulators, Disease Models, Animal, Dose-Response Relationship, Drug, Male, Rats, Rats, Sprague-Dawley, Receptors, Cannabinoid, Time Factors.
Abstract
The present study was designed to determine the potential of CB1 cannabinoid receptor modulating compounds in the treatment of L‐3,4‐dihydroxyphenylalanine (L‐dopa)–induced dyskinesia in Parkinson's disease. In the reserpine‐treated rat model of parkinsonism, administration of a high dose of L‐dopa (150 mg/kg) but not of Cl‐APB (0.5 mg/kg) or quinpirole (0.5 mg/kg) produced a hyperkinetic state characterised by an increase in horizontal and vertical activity, which likely represent correlates of antiparkinsonian and dyskinetic activity, respectively. Injection of the CB1 cannabinoid receptor antagonist SR141716 (0.1–3 mg/kg) reduced the increase in vertical activity elicited by L‐dopa without affecting the increase in horizontal activity. Injection of the CB1 cannabinoid receptor agonist WIN55,212‐2 (0.1–3 mg/kg) reduced the L‐dopa–induced increase in vertical activity and, at the highest dose only (3 mg/kg), also reduced horizontal activity elicited by L‐dopa. WIN55,212‐2 (1 mg/kg) reduced motor activity induced by both the D1 receptor agonist Cl‐APB (0.5 mg/kg) and the D2 receptor agonist quinpirole (0.5 mg/kg) in the reserpine‐treated rat. SR141716 (1 mg/kg) had no effects on motor activity induced by Cl‐APB (0.5 mg/kg) nor quinpirole (0.5 mg/kg) in the reserpine‐treated rat. Injection of the inhibitor of endocannabinoid transport AM404 (0.1–1 mg/kg) did not affect the increase in horizontal or vertical activity elicited by L‐dopa (150 mg/kg) in the reserpine‐treated rat. The data suggest that both CB1 cannabinoid receptor antagonists and agonists can modulate the behavioural effects of L‐dopa and may be useful for the treatment of the dyskinesia associated with long‐term L‐dopa treatment of Parkinson's disease. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10312
Affiliations:
- Espagne, Royaume-Uni
- Angleterre, Communauté de Madrid, Grand Manchester
- Madrid, Manchester
- Université de Manchester
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Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>New York</pubPlace><date type="published" when="2003-02">2003-02</date><biblScope unit="vol">18</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="138">138</biblScope><biblScope unit="page" to="149">149</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E717F6FBFBFE610C70E9A45BF13EE32A44CB41DA</idno><idno type="DOI">10.1002/mds.10312</idno><idno type="ArticleID">MDS10312</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenergic Uptake Inhibitors (therapeutic use)</term><term>Alkaloid</term><term>Animal</term><term>Animal model</term><term>Animals</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson agent</term><term>Behavior, Animal (drug effects)</term><term>CB1 cannabinoid receptor</term><term>CB1 receptors</term><term>Cannabinoid Receptor Modulators</term><term>Disease Models, Animal</term><term>Dose-Response Relationship, Drug</term><term>Fatty Acids, Unsaturated (pharmacology)</term><term>Hyperkinesia</term><term>Hyperkinesis (chemically induced)</term><term>Levodopa</term><term>Levodopa (administration & dosage)</term><term>Levodopa (adverse effects)</term><term>L‐dopa</term><term>Male</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson disease</term><term>Pathophysiology</term><term>Rat</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Receptors, Cannabinoid</term><term>Receptors, Drug (drug effects)</term><term>Reserpine</term><term>Reserpine (therapeutic use)</term><term>Time Factors</term><term>cannabinoids</term><term>dyskinesia</term><term>reserpine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</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="drug effects" xml:lang="en"><term>Receptors, Drug</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Fatty Acids, Unsaturated</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Adrenergic Uptake Inhibitors</term><term>Reserpine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Hyperkinesis</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Behavior, Animal</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cannabinoid Receptor Modulators</term><term>Disease Models, Animal</term><term>Dose-Response Relationship, Drug</term><term>Male</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Receptors, Cannabinoid</term><term>Time Factors</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Alcaloïde</term><term>Animal</term><term>Antiparkinsonien</term><term>Hyperkinésie</term><term>Lévodopa</term><term>Modèle animal</term><term>Parkinson maladie</term><term>Physiopathologie</term><term>Rat</term><term>Récepteur cannabinoïde CB1</term><term>Réserpine</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The present study was designed to determine the potential of CB1 cannabinoid receptor modulating compounds in the treatment of L‐3,4‐dihydroxyphenylalanine (L‐dopa)–induced dyskinesia in Parkinson's disease. In the reserpine‐treated rat model of parkinsonism, administration of a high dose of L‐dopa (150 mg/kg) but not of Cl‐APB (0.5 mg/kg) or quinpirole (0.5 mg/kg) produced a hyperkinetic state characterised by an increase in horizontal and vertical activity, which likely represent correlates of antiparkinsonian and dyskinetic activity, respectively. Injection of the CB1 cannabinoid receptor antagonist SR141716 (0.1–3 mg/kg) reduced the increase in vertical activity elicited by L‐dopa without affecting the increase in horizontal activity. Injection of the CB1 cannabinoid receptor agonist WIN55,212‐2 (0.1–3 mg/kg) reduced the L‐dopa–induced increase in vertical activity and, at the highest dose only (3 mg/kg), also reduced horizontal activity elicited by L‐dopa. WIN55,212‐2 (1 mg/kg) reduced motor activity induced by both the D1 receptor agonist Cl‐APB (0.5 mg/kg) and the D2 receptor agonist quinpirole (0.5 mg/kg) in the reserpine‐treated rat. SR141716 (1 mg/kg) had no effects on motor activity induced by Cl‐APB (0.5 mg/kg) nor quinpirole (0.5 mg/kg) in the reserpine‐treated rat. Injection of the inhibitor of endocannabinoid transport AM404 (0.1–1 mg/kg) did not affect the increase in horizontal or vertical activity elicited by L‐dopa (150 mg/kg) in the reserpine‐treated rat. The data suggest that both CB1 cannabinoid receptor antagonists and agonists can modulate the behavioural effects of L‐dopa and may be useful for the treatment of the dyskinesia associated with long‐term L‐dopa treatment of Parkinson's disease. © 2002 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Espagne</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Communauté de Madrid</li><li>Grand Manchester</li></region><settlement><li>Madrid</li><li>Manchester</li></settlement><orgName><li>Université de Manchester</li></orgName></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Segovia, Gregorio" sort="Segovia, Gregorio" uniqKey="Segovia G" first="Gregorio" last="Segovia">Gregorio Segovia</name></region><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name><name sortKey="Crossman, Alan R" sort="Crossman, Alan R" uniqKey="Crossman A" first="Alan R." last="Crossman">Alan R. Crossman</name><name sortKey="Crossman, Alan R" sort="Crossman, Alan R" uniqKey="Crossman A" first="Alan R." last="Crossman">Alan R. Crossman</name></country><country name="Espagne"><region name="Communauté de Madrid"><name sortKey="Segovia, Gregorio" sort="Segovia, Gregorio" uniqKey="Segovia G" first="Gregorio" last="Segovia">Gregorio Segovia</name></region><name sortKey="Mora, Francisco" sort="Mora, Francisco" uniqKey="Mora F" first="Francisco" last="Mora">Francisco Mora</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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