Stimulation of cannabinoid receptors reduces levodopa-induced dyskinesia in the MPTP-lesioned nonhuman primate model of Parkinson's disease.
Identifieur interne : 003924 ( PubMed/Curation ); précédent : 003923; suivant : 003925Stimulation of cannabinoid receptors reduces levodopa-induced dyskinesia in the MPTP-lesioned nonhuman primate model of Parkinson's disease.
Auteurs : Susan H. Fox [Royaume-Uni] ; Brian Henry ; Michael Hill ; Alan Crossman ; Jonathan BrotchieSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2002.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animals, Antiparkinson Agents (toxicity), Benserazide (toxicity), Callithrix, Corpus Striatum (drug effects), Corpus Striatum (physiopathology), Dose-Response Relationship, Drug, Dronabinol (analogs & derivatives), Dronabinol (pharmacology), Drug Combinations, Drug Therapy, Combination, Dyskinesia, Drug-Induced (physiopathology), Female, Globus Pallidus (drug effects), Globus Pallidus (physiopathology), Levodopa (toxicity), Male, Motor Skills (drug effects), Parkinsonian Disorders (physiopathology), Receptors, Cannabinoid, Receptors, Drug (drug effects), Receptors, Drug (physiology), gamma-Aminobutyric Acid (metabolism).
- MESH :
- chemical , analogs & derivatives : Dronabinol.
- chemical , drug effects : Receptors, Drug.
- chemical , metabolism : gamma-Aminobutyric Acid.
- chemical , pharmacology : Dronabinol.
- chemical , physiology : Receptors, Drug.
- chemical , toxicity : Antiparkinson Agents, Benserazide, Levodopa.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Drug Combinations, Receptors, Cannabinoid.
- drug effects : Corpus Striatum, Globus Pallidus, Motor Skills.
- physiopathology : Corpus Striatum, Dyskinesia, Drug-Induced, Globus Pallidus, Parkinsonian Disorders.
- Animals, Callithrix, Dose-Response Relationship, Drug, Drug Therapy, Combination, Female, Male.
Abstract
Long-term treatment with levodopa in Parkinson's disease results in the development of motor fluctuations, including reduced duration of antiparkinsonian action and involuntary movements, i.e., levodopa-induced dyskinesia. Cannabinoid receptors are concentrated in the basal ganglia, and stimulation of cannabinoid receptors can increase gamma-aminobutyric acid transmission in the lateral segment of globus pallidus and reduce glutamate release in the striatum. We thus tested the hypothesis that the cannabinoid receptor agonist nabilone (0.01, 0.03, and 0.10 mg/kg) would alleviate levodopa-induced dyskinesia in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) -lesioned marmoset model of Parkinson's disease. Coadministration of nabilone (0.1 mg/kg) with levodopa was associated with significantly less total dyskinesia (dyskinesia score, 12; range, 6-17; primate dyskinesia rating scale) than levodopa alone (22; range, 14-23; P < 0.05). This effect was more marked during the onset period (0-20 minutes post levodopa). There was no reduction in the antiparkinsonian action of levodopa. Furthermore, the intermediate dose of nabilone used (0.03 mg/kg) increased the duration of antiparkinsonian action of levodopa by 76%. Thus, cannabinoid receptor agonists may be useful in the treatment of motor complications in Parkinson's disease.
DOI: 10.1002/mds.10289
PubMed: 12465055
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pubmed:12465055Le document en format XML
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Fox</name><affiliation wicri:level="1"><nlm:affiliation>Manchester Movement Disorder Laboratory, Division of Neuroscience, School of Biological Sciences, University of Manchester, Oxford Road, Manchester, United Kingdom. shfox@hotmail.com</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Manchester Movement Disorder Laboratory, Division of Neuroscience, School of Biological Sciences, University of Manchester, Oxford Road, Manchester</wicri:regionArea></affiliation></author><author><name sortKey="Henry, Brian" sort="Henry, Brian" uniqKey="Henry B" first="Brian" last="Henry">Brian Henry</name></author><author><name sortKey="Hill, Michael" sort="Hill, Michael" uniqKey="Hill M" first="Michael" last="Hill">Michael Hill</name></author><author><name sortKey="Crossman, Alan" sort="Crossman, Alan" uniqKey="Crossman A" first="Alan" last="Crossman">Alan Crossman</name></author><author><name sortKey="Brotchie, Jonathan" sort="Brotchie, Jonathan" uniqKey="Brotchie J" first="Jonathan" last="Brotchie">Jonathan Brotchie</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:12465055</idno><idno type="pmid">12465055</idno><idno type="doi">10.1002/mds.10289</idno><idno type="wicri:Area/PubMed/Corpus">003924</idno><idno type="wicri:Area/PubMed/Curation">003924</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Stimulation of cannabinoid receptors reduces levodopa-induced dyskinesia in the MPTP-lesioned nonhuman primate model of Parkinson's disease.</title><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. Fox</name><affiliation wicri:level="1"><nlm:affiliation>Manchester Movement Disorder Laboratory, Division of Neuroscience, School of Biological Sciences, University of Manchester, Oxford Road, Manchester, United Kingdom. shfox@hotmail.com</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Manchester Movement Disorder Laboratory, Division of Neuroscience, School of Biological Sciences, University of Manchester, Oxford Road, Manchester</wicri:regionArea></affiliation></author><author><name sortKey="Henry, Brian" sort="Henry, Brian" uniqKey="Henry B" first="Brian" last="Henry">Brian Henry</name></author><author><name sortKey="Hill, Michael" sort="Hill, Michael" uniqKey="Hill M" first="Michael" last="Hill">Michael Hill</name></author><author><name sortKey="Crossman, Alan" sort="Crossman, Alan" uniqKey="Crossman A" first="Alan" last="Crossman">Alan Crossman</name></author><author><name sortKey="Brotchie, Jonathan" sort="Brotchie, Jonathan" uniqKey="Brotchie J" first="Jonathan" last="Brotchie">Jonathan Brotchie</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Animals</term><term>Antiparkinson Agents (toxicity)</term><term>Benserazide (toxicity)</term><term>Callithrix</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (physiopathology)</term><term>Dose-Response Relationship, Drug</term><term>Dronabinol (analogs & derivatives)</term><term>Dronabinol (pharmacology)</term><term>Drug Combinations</term><term>Drug Therapy, Combination</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Female</term><term>Globus Pallidus (drug effects)</term><term>Globus Pallidus (physiopathology)</term><term>Levodopa (toxicity)</term><term>Male</term><term>Motor Skills (drug effects)</term><term>Parkinsonian Disorders (physiopathology)</term><term>Receptors, Cannabinoid</term><term>Receptors, Drug (drug effects)</term><term>Receptors, Drug (physiology)</term><term>gamma-Aminobutyric Acid (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Dronabinol</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, Drug</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>gamma-Aminobutyric Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dronabinol</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, Drug</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Antiparkinson Agents</term><term>Benserazide</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Drug Combinations</term><term>Receptors, Cannabinoid</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Corpus Striatum</term><term>Globus Pallidus</term><term>Motor Skills</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term><term>Dyskinesia, Drug-Induced</term><term>Globus Pallidus</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Callithrix</term><term>Dose-Response Relationship, Drug</term><term>Drug Therapy, Combination</term><term>Female</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Long-term treatment with levodopa in Parkinson's disease results in the development of motor fluctuations, including reduced duration of antiparkinsonian action and involuntary movements, i.e., levodopa-induced dyskinesia. Cannabinoid receptors are concentrated in the basal ganglia, and stimulation of cannabinoid receptors can increase gamma-aminobutyric acid transmission in the lateral segment of globus pallidus and reduce glutamate release in the striatum. We thus tested the hypothesis that the cannabinoid receptor agonist nabilone (0.01, 0.03, and 0.10 mg/kg) would alleviate levodopa-induced dyskinesia in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) -lesioned marmoset model of Parkinson's disease. Coadministration of nabilone (0.1 mg/kg) with levodopa was associated with significantly less total dyskinesia (dyskinesia score, 12; range, 6-17; primate dyskinesia rating scale) than levodopa alone (22; range, 14-23; P < 0.05). This effect was more marked during the onset period (0-20 minutes post levodopa). There was no reduction in the antiparkinsonian action of levodopa. Furthermore, the intermediate dose of nabilone used (0.03 mg/kg) increased the duration of antiparkinsonian action of levodopa by 76%. Thus, cannabinoid receptor agonists may be useful in the treatment of motor complications in Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">12465055</PMID><DateCreated><Year>2002</Year><Month>12</Month><Day>04</Day></DateCreated><DateCompleted><Year>2003</Year><Month>03</Month><Day>24</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>17</Volume><Issue>6</Issue><PubDate><Year>2002</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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We thus tested the hypothesis that the cannabinoid receptor agonist nabilone (0.01, 0.03, and 0.10 mg/kg) would alleviate levodopa-induced dyskinesia in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) -lesioned marmoset model of Parkinson's disease. Coadministration of nabilone (0.1 mg/kg) with levodopa was associated with significantly less total dyskinesia (dyskinesia score, 12; range, 6-17; primate dyskinesia rating scale) than levodopa alone (22; range, 14-23; P < 0.05). This effect was more marked during the onset period (0-20 minutes post levodopa). There was no reduction in the antiparkinsonian action of levodopa. Furthermore, the intermediate dose of nabilone used (0.03 mg/kg) increased the duration of antiparkinsonian action of levodopa by 76%. 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UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005917">Globus Pallidus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000633">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009048">Motor Skills</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020734">Parkinsonian Disorders</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D043882">Receptors, Cannabinoid</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011955">Receptors, Drug</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005680">gamma-Aminobutyric Acid</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>12</Month><Day>5</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2003</Year><Month>3</Month><Day>26</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>12</Month><Day>5</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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