Neural mechanisms of dystonia: evidence from a 2-deoxyglucose uptake study in a primate model of dopamine agonist-induced dystonia.
Identifieur interne : 004F04 ( PubMed/Corpus ); précédent : 004F03; suivant : 004F05Neural mechanisms of dystonia: evidence from a 2-deoxyglucose uptake study in a primate model of dopamine agonist-induced dystonia.
Auteurs : I J Mitchell ; R. Luquin ; S. Boyce ; C E Clarke ; R G Robertson ; M A Sambrook ; A R CrossmanSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1990.
English descriptors
- KwdEn :
- Animals, Apomorphine (adverse effects), Apomorphine (therapeutic use), Deoxy Sugars (pharmacokinetics), Deoxyglucose (pharmacokinetics), Dystonia (chemically induced), Dystonia (metabolism), MPTP Poisoning, Macaca fascicularis, Male, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (complications).
- 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.
DOI: 10.1002/mds.870050113
PubMed: 2296259
Links to Exploration step
pubmed:2296259Le document en format XML
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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, A R" sort="Crossman, A R" uniqKey="Crossman A" first="A R" last="Crossman">A R Crossman</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1990">1990</date><idno type="RBID">pubmed:2296259</idno><idno type="pmid">2296259</idno><idno type="doi">10.1002/mds.870050113</idno><idno type="wicri:Area/PubMed/Corpus">004F04</idno></publicationStmt><sourceDesc><biblStruct><analytic><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><affiliation><nlm:affiliation>Department of Cell and Structural Biology, School of Biological Sciences, University of Manchester, England.</nlm:affiliation></affiliation></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, A R" sort="Crossman, A R" uniqKey="Crossman A" first="A R" last="Crossman">A R Crossman</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="1990" type="published">1990</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apomorphine (adverse effects)</term><term>Apomorphine (therapeutic use)</term><term>Deoxy Sugars (pharmacokinetics)</term><term>Deoxyglucose (pharmacokinetics)</term><term>Dystonia (chemically induced)</term><term>Dystonia (metabolism)</term><term>MPTP Poisoning</term><term>Macaca fascicularis</term><term>Male</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (complications)</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></textClass></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><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">2296259</PMID><DateCreated><Year>1990</Year><Month>02</Month><Day>16</Day></DateCreated><DateCompleted><Year>1990</Year><Month>02</Month><Day>16</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>5</Volume><Issue>1</Issue><PubDate><Year>1990</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Neural mechanisms of dystonia: evidence from a 2-deoxyglucose uptake study in a primate model of dopamine agonist-induced dystonia.</ArticleTitle><Pagination><MedlinePgn>49-54</MedlinePgn></Pagination><Abstract><AbstractText>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). 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