Neural mechanisms of dystonia: Evidence from a 2‐deoxyglucose uptake study in a primate model of dopamine agonist‐induced dystonia
Identifieur interne : 006296 ( Main/Exploration ); précédent : 006295; suivant : 006297Neural mechanisms of dystonia: Evidence from a 2‐deoxyglucose uptake study in a primate model of dopamine agonist‐induced dystonia
Auteurs : I. J. Mitchell [Royaume-Uni] ; R. Luquin [Espagne] ; S. Boyce [Royaume-Uni] ; C. E. Clarke [Royaume-Uni] ; R. G. Robertson [Royaume-Uni] ; M. A. Sambrook [Royaume-Uni] ; Crossman [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1990.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Cartographie, Singe.
English descriptors
- KwdEn :
- 2‐Deoxyglucose uptake, Animal, Animals, Apomorphine (adverse effects), Apomorphine (therapeutic use), Autoradiography, Brain, Cartography, Densitometry, Deoxy Sugars (pharmacokinetics), Deoxyglucose (pharmacokinetics), Dopamine agonist, Dopamine antagonist, Dystonia, Dystonia (chemically induced), Dystonia (metabolism), Experimental disease, Extrapyramidal syndrome, MPTP Poisoning, Macaca fascicularis, Male, Monkey, Nervous system diseases, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (complications), Pathogenesis, Primate model, Radionuclide study.
- MESH :
- chemical , adverse effects : Apomorphine.
- chemical , pharmacokinetics : Deoxy Sugars, Deoxyglucose.
- chemical , therapeutic use : Apomorphine.
- chemically induced : Dystonia, Parkinson Disease, Secondary.
- complications : Parkinson Disease, Secondary.
- metabolism : Dystonia.
- Animals, MPTP Poisoning, Macaca fascicularis, Male.
Abstract
The neural mechanisms that mediate dystonia were investigated in a novel experimental primate model of dopamine agonist‐induced dystonia. This condition was produced by long‐term (15 months) dopamine agonist therapy of a macaque monkey that had been rendered hemiparkinsonian by unilateral infusion of 1–methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine into the right common carotid artery. The 2–deoxyglucose (2–DG) metabolic mapping technique was applied to the animal during the expression of active unilateral dystonia, and regional brain uptake of 2–DG was assessed autoradiographically. The results demonstrate that dystonia is associated with marked increases in 2–DG uptake in the constituent nuclei of the basal ganglia (caudate nucleus, putamen, medial and lateral segments of the globus pallidus) and in the subthalamic nucleus, but decreased uptake in the structures that receive output of the basal ganglia (ventral anterior/ventral lateral thalamic complex and lateral habenula). Based on these findings it is suggested that dystonia is characterized by increased activity in the putaminopallidal and pallidosubthalamic pathways, and decreased activity in the subthalamopallidal and pallidothalamic pathways.
Url:
DOI: 10.1002/mds.870050113
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 002963
- to stream Istex, to step Curation: 002963
- to stream Istex, to step Checkpoint: 004385
- to stream PubMed, to step Corpus: 004F04
- to stream PubMed, to step Curation: 004F04
- to stream PubMed, to step Checkpoint: 004E95
- to stream Ncbi, to step Merge: 003798
- to stream Ncbi, to step Curation: 003798
- to stream Ncbi, to step Checkpoint: 003798
- to stream Main, to step Merge: 009630
- to stream PascalFrancis, to step Corpus: 003A14
- to stream PascalFrancis, to step Curation: 002E11
- to stream PascalFrancis, to step Checkpoint: 003937
- to stream Main, to step Merge: 009713
- to stream Main, to step Curation: 006296
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neural mechanisms of dystonia: Evidence from a 2‐deoxyglucose uptake study in a primate model of dopamine agonist‐induced dystonia</title><author><name sortKey="Mitchell, I J" sort="Mitchell, I J" uniqKey="Mitchell I" first="I. J." last="Mitchell">I. J. Mitchell</name></author><author><name sortKey="Luquin, R" sort="Luquin, R" uniqKey="Luquin R" first="R." last="Luquin">R. Luquin</name></author><author><name sortKey="Boyce, S" sort="Boyce, S" uniqKey="Boyce S" first="S." last="Boyce">S. Boyce</name></author><author><name sortKey="Clarke, C E" sort="Clarke, C E" uniqKey="Clarke C" first="C. E." last="Clarke">C. E. Clarke</name></author><author><name sortKey="Robertson, R G" sort="Robertson, R G" uniqKey="Robertson R" first="R. G." last="Robertson">R. G. Robertson</name></author><author><name sortKey="Sambrook, M A" sort="Sambrook, M A" uniqKey="Sambrook M" first="M. A." last="Sambrook">M. A. Sambrook</name></author><author><name sortKey="Crossman" sort="Crossman" uniqKey="Crossman" last="Crossman">Crossman</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:7A6813D6CF951BAAE92D307917D2096C89487314</idno><date when="1990" year="1990">1990</date><idno type="doi">10.1002/mds.870050113</idno><idno type="url">https://api.istex.fr/document/7A6813D6CF951BAAE92D307917D2096C89487314/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002963</idno><idno type="wicri:Area/Istex/Curation">002963</idno><idno type="wicri:Area/Istex/Checkpoint">004385</idno><idno type="wicri:doubleKey">0885-3185:1990:Mitchell I:neural:mechanisms:of</idno><idno type="wicri:source">PubMed</idno><idno type="RBID">pubmed:2296259</idno><idno type="wicri:Area/PubMed/Corpus">004F04</idno><idno type="wicri:Area/PubMed/Curation">004F04</idno><idno type="wicri:Area/PubMed/Checkpoint">004E95</idno><idno type="wicri:Area/Ncbi/Merge">003798</idno><idno type="wicri:Area/Ncbi/Curation">003798</idno><idno type="wicri:Area/Ncbi/Checkpoint">003798</idno><idno type="wicri:doubleKey">0885-3185:1990:Mitchell I:neural:mechanisms:of</idno><idno type="wicri:Area/Main/Merge">009630</idno><idno type="wicri:source">INIST</idno><idno type="RBID">Pascal:90-0127385</idno><idno type="wicri:Area/PascalFrancis/Corpus">003A14</idno><idno type="wicri:Area/PascalFrancis/Curation">002E11</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">003937</idno><idno type="wicri:doubleKey">0885-3185:1990:Mitchell I:neural:mechanisms:of</idno><idno type="wicri:Area/Main/Merge">009713</idno><idno type="wicri:Area/Main/Curation">006296</idno><idno type="wicri:Area/Main/Exploration">006296</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neural mechanisms of dystonia: Evidence from a 2‐deoxyglucose uptake study in a primate model of dopamine agonist‐induced dystonia</title><author><name sortKey="Mitchell, I J" sort="Mitchell, I J" uniqKey="Mitchell I" first="I. J." last="Mitchell">I. J. Mitchell</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Experimental Neurology Group, Department of Cell and Structural Biology, School of Biological Sciences, University of Manchester, Manchester</wicri:cityArea></affiliation></author><author><name sortKey="Luquin, R" sort="Luquin, R" uniqKey="Luquin R" first="R." last="Luquin">R. Luquin</name><affiliation wicri:level="1"><country xml:lang="fr">Espagne</country><wicri:regionArea>Department of Neurology, University Clinic, University of Navarra Medical School, Pamplona</wicri:regionArea><wicri:noRegion>Pamplona</wicri:noRegion></affiliation></author><author><name sortKey="Boyce, S" sort="Boyce, S" uniqKey="Boyce S" first="S." last="Boyce">S. Boyce</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Merck, Sharp and Dohme Research Laboratories, Harlow, Essex</wicri:cityArea></affiliation></author><author><name sortKey="Clarke, C E" sort="Clarke, C E" uniqKey="Clarke C" first="C. E." last="Clarke">C. E. Clarke</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Experimental Neurology Group, Department of Cell and Structural Biology, School of Biological Sciences, University of Manchester, Manchester</wicri:cityArea></affiliation></author><author><name sortKey="Robertson, R G" sort="Robertson, R G" uniqKey="Robertson R" first="R. G." last="Robertson">R. G. Robertson</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Experimental Neurology Group, Department of Cell and Structural Biology, School of Biological Sciences, University of Manchester, Manchester</wicri:cityArea></affiliation></author><author><name sortKey="Sambrook, M A" sort="Sambrook, M A" uniqKey="Sambrook M" first="M. A." last="Sambrook">M. A. Sambrook</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Experimental Neurology Group, Department of Cell and Structural Biology, School of Biological Sciences, University of Manchester, Manchester</wicri:cityArea></affiliation></author><author><name sortKey="Crossman" sort="Crossman" uniqKey="Crossman" last="Crossman">Crossman</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Experimental Neurology Group, Department of Cell and Structural Biology, School of Biological Sciences, University of Manchester, Manchester</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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>Hoboken</pubPlace><date type="published" when="1990">1990</date><biblScope unit="vol">5</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="49">49</biblScope><biblScope unit="page" to="54">54</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">7A6813D6CF951BAAE92D307917D2096C89487314</idno><idno type="DOI">10.1002/mds.870050113</idno><idno type="ArticleID">MDS870050113</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>2‐Deoxyglucose uptake</term><term>Animal</term><term>Animals</term><term>Apomorphine (adverse effects)</term><term>Apomorphine (therapeutic use)</term><term>Autoradiography</term><term>Brain</term><term>Cartography</term><term>Densitometry</term><term>Deoxy Sugars (pharmacokinetics)</term><term>Deoxyglucose (pharmacokinetics)</term><term>Dopamine agonist</term><term>Dopamine antagonist</term><term>Dystonia</term><term>Dystonia (chemically induced)</term><term>Dystonia (metabolism)</term><term>Experimental disease</term><term>Extrapyramidal syndrome</term><term>MPTP Poisoning</term><term>Macaca fascicularis</term><term>Male</term><term>Monkey</term><term>Nervous system diseases</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (complications)</term><term>Pathogenesis</term><term>Primate model</term><term>Radionuclide study</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Apomorphine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Deoxy Sugars</term><term>Deoxyglucose</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Apomorphine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Dystonia</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dystonia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>MPTP Poisoning</term><term>Macaca fascicularis</term><term>Male</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Animal</term><term>Antagoniste dopamine</term><term>Autoradiographie</term><term>Cartographie</term><term>Densitométrie</term><term>Dystonie</term><term>Encéphale</term><term>Exploration radioisotopique</term><term>Extrapyramidal syndrome</term><term>Glucose(désoxy-2)</term><term>MPTP</term><term>Pathogénie</term><term>Pathologie expérimentale</term><term>Singe</term><term>Système nerveux pathologie</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Cartographie</term><term>Singe</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The neural mechanisms that mediate dystonia were investigated in a novel experimental primate model of dopamine agonist‐induced dystonia. This condition was produced by long‐term (15 months) dopamine agonist therapy of a macaque monkey that had been rendered hemiparkinsonian by unilateral infusion of 1–methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine into the right common carotid artery. The 2–deoxyglucose (2–DG) metabolic mapping technique was applied to the animal during the expression of active unilateral dystonia, and regional brain uptake of 2–DG was assessed autoradiographically. The results demonstrate that dystonia is associated with marked increases in 2–DG uptake in the constituent nuclei of the basal ganglia (caudate nucleus, putamen, medial and lateral segments of the globus pallidus) and in the subthalamic nucleus, but decreased uptake in the structures that receive output of the basal ganglia (ventral anterior/ventral lateral thalamic complex and lateral habenula). Based on these findings it is suggested that dystonia is characterized by increased activity in the putaminopallidal and pallidosubthalamic pathways, and decreased activity in the subthalamopallidal and pallidothalamic pathways.</div></front></TEI><affiliations><list><country><li>Espagne</li><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Mitchell, I J" sort="Mitchell, I J" uniqKey="Mitchell I" first="I. J." last="Mitchell">I. J. Mitchell</name></region><name sortKey="Boyce, S" sort="Boyce, S" uniqKey="Boyce S" first="S." last="Boyce">S. Boyce</name><name sortKey="Clarke, C E" sort="Clarke, C E" uniqKey="Clarke C" first="C. E." last="Clarke">C. E. Clarke</name><name sortKey="Crossman" sort="Crossman" uniqKey="Crossman" last="Crossman">Crossman</name><name sortKey="Robertson, R G" sort="Robertson, R G" uniqKey="Robertson R" first="R. G." last="Robertson">R. G. Robertson</name><name sortKey="Sambrook, M A" sort="Sambrook, M A" uniqKey="Sambrook M" first="M. A." last="Sambrook">M. A. Sambrook</name></country><country name="Espagne"><noRegion><name sortKey="Luquin, R" sort="Luquin, R" uniqKey="Luquin R" first="R." last="Luquin">R. Luquin</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 006296 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 006296 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:7A6813D6CF951BAAE92D307917D2096C89487314
|texte= Neural mechanisms of dystonia: Evidence from a 2‐deoxyglucose uptake study in a primate model of dopamine agonist‐induced dystonia
}}
| This area was generated with Dilib version V0.6.23. |  |