Regional changes in 2-deoxyglucose uptake associated with neuroleptic-induced tardive dyskinesia in the Cebus monkey.
Identifieur interne : 004D12 ( PubMed/Checkpoint ); précédent : 004D11; suivant : 004D13Regional changes in 2-deoxyglucose uptake associated with neuroleptic-induced tardive dyskinesia in the Cebus monkey.
Auteurs : I J Mitchell [Royaume-Uni] ; A R Crossman ; U. Liminga ; P. Andren ; L M GunneSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1992.
English descriptors
- KwdEn :
- Animals, Autoradiography, Blood Glucose (metabolism), Brain (drug effects), Brain (pathology), Brain Mapping, Cebus, Densitometry, Deoxyglucose (metabolism), Dyskinesia, Drug-Induced (pathology), Fluphenazine (analogs & derivatives), Fluphenazine (toxicity), Globus Pallidus (drug effects), Globus Pallidus (pathology), Thalamic Nuclei (drug effects), Thalamic Nuclei (pathology).
- MESH :
- chemical , analogs & derivatives : Fluphenazine.
- chemical , metabolism : Blood Glucose, Deoxyglucose.
- drug effects : Brain, Globus Pallidus, Thalamic Nuclei.
- pathology : Brain, Dyskinesia, Drug-Induced, Globus Pallidus, Thalamic Nuclei.
- chemical , toxicity : Fluphenazine.
- Animals, Autoradiography, Brain Mapping, Cebus, Densitometry.
Abstract
The neural mechanisms that mediate a primate model of tardive dyskinesia have been investigated using the 2-deoxyglucose (2-DG) uptake technique. Three groups of Cebus monkeys were used. Some of the animals received long-term neuroleptic treatment. These animals were allotted to one of two groups depending on whether they developed tardive dyskinesia or not. A third group of animals served as untreated controls. The neuroleptic-treated dyskinetic animals showed reduced uptake of 2-DG in the medial segment of the globus pallidus and in the ventral anterior (VA) and ventral lateral (VL) nuclei of the thalamus relative to that seen in the equivalent structures in the neuroleptic-treated nondyskinetic and untreated control animals. The data are interpreted as suggesting that tardive dyskinesia is mediated by underactivity of the pathways from the subthalamic nucleus to the medial pallidal segment and the substantia pars nigra pars reticulata, which in turn result in a loss of gamma-aminobutyric acid-ergic inhibition of the VA and VL thalamic nuclei. This suggests that tardive dyskinesia shares a common underlying neural mechanism with other hyperkinesias such as chorea and ballism.
DOI: 10.1002/mds.870070106
PubMed: 1557064
Affiliations:
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Liminga</name></author><author><name sortKey="Andren, P" sort="Andren, P" uniqKey="Andren P" first="P" last="Andren">P. Andren</name></author><author><name sortKey="Gunne, L M" sort="Gunne, L M" uniqKey="Gunne L" first="L M" last="Gunne">L M Gunne</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1992">1992</date><idno type="RBID">pubmed:1557064</idno><idno type="pmid">1557064</idno><idno type="doi">10.1002/mds.870070106</idno><idno type="wicri:Area/PubMed/Corpus">004D60</idno><idno type="wicri:Area/PubMed/Curation">004D60</idno><idno type="wicri:Area/PubMed/Checkpoint">004D12</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Regional changes in 2-deoxyglucose uptake associated with neuroleptic-induced tardive dyskinesia in the Cebus monkey.</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"><nlm:affiliation>Department of Cell and Structural Biology, University of Manchester, England.</nlm:affiliation><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Cell and Structural Biology, University of Manchester</wicri:cityArea></affiliation></author><author><name sortKey="Crossman, A R" sort="Crossman, A R" uniqKey="Crossman A" first="A R" last="Crossman">A R Crossman</name></author><author><name sortKey="Liminga, U" sort="Liminga, U" uniqKey="Liminga U" first="U" last="Liminga">U. Liminga</name></author><author><name sortKey="Andren, P" sort="Andren, P" uniqKey="Andren P" first="P" last="Andren">P. Andren</name></author><author><name sortKey="Gunne, L M" sort="Gunne, L M" uniqKey="Gunne L" first="L M" last="Gunne">L M Gunne</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="1992" type="published">1992</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autoradiography</term><term>Blood Glucose (metabolism)</term><term>Brain (drug effects)</term><term>Brain (pathology)</term><term>Brain Mapping</term><term>Cebus</term><term>Densitometry</term><term>Deoxyglucose (metabolism)</term><term>Dyskinesia, Drug-Induced (pathology)</term><term>Fluphenazine (analogs & derivatives)</term><term>Fluphenazine (toxicity)</term><term>Globus Pallidus (drug effects)</term><term>Globus Pallidus (pathology)</term><term>Thalamic Nuclei (drug effects)</term><term>Thalamic Nuclei (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Fluphenazine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Blood Glucose</term><term>Deoxyglucose</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term><term>Globus Pallidus</term><term>Thalamic Nuclei</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Dyskinesia, Drug-Induced</term><term>Globus Pallidus</term><term>Thalamic Nuclei</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Fluphenazine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Autoradiography</term><term>Brain Mapping</term><term>Cebus</term><term>Densitometry</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The neural mechanisms that mediate a primate model of tardive dyskinesia have been investigated using the 2-deoxyglucose (2-DG) uptake technique. Three groups of Cebus monkeys were used. Some of the animals received long-term neuroleptic treatment. These animals were allotted to one of two groups depending on whether they developed tardive dyskinesia or not. A third group of animals served as untreated controls. The neuroleptic-treated dyskinetic animals showed reduced uptake of 2-DG in the medial segment of the globus pallidus and in the ventral anterior (VA) and ventral lateral (VL) nuclei of the thalamus relative to that seen in the equivalent structures in the neuroleptic-treated nondyskinetic and untreated control animals. The data are interpreted as suggesting that tardive dyskinesia is mediated by underactivity of the pathways from the subthalamic nucleus to the medial pallidal segment and the substantia pars nigra pars reticulata, which in turn result in a loss of gamma-aminobutyric acid-ergic inhibition of the VA and VL thalamic nuclei. This suggests that tardive dyskinesia shares a common underlying neural mechanism with other hyperkinesias such as chorea and ballism.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">1557064</PMID><DateCreated><Year>1992</Year><Month>05</Month><Day>04</Day></DateCreated><DateCompleted><Year>1992</Year><Month>05</Month><Day>04</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>7</Volume><Issue>1</Issue><PubDate><Year>1992</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Regional changes in 2-deoxyglucose uptake associated with neuroleptic-induced tardive dyskinesia in the Cebus monkey.</ArticleTitle><Pagination><MedlinePgn>32-7</MedlinePgn></Pagination><Abstract><AbstractText>The neural mechanisms that mediate a primate model of tardive dyskinesia have been investigated using the 2-deoxyglucose (2-DG) uptake technique. Three groups of Cebus monkeys were used. Some of the animals received long-term neuroleptic treatment. These animals were allotted to one of two groups depending on whether they developed tardive dyskinesia or not. A third group of animals served as untreated controls. The neuroleptic-treated dyskinetic animals showed reduced uptake of 2-DG in the medial segment of the globus pallidus and in the ventral anterior (VA) and ventral lateral (VL) nuclei of the thalamus relative to that seen in the equivalent structures in the neuroleptic-treated nondyskinetic and untreated control animals. The data are interpreted as suggesting that tardive dyskinesia is mediated by underactivity of the pathways from the subthalamic nucleus to the medial pallidal segment and the substantia pars nigra pars reticulata, which in turn result in a loss of gamma-aminobutyric acid-ergic inhibition of the VA and VL thalamic nuclei. 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Andren</name><name sortKey="Crossman, A R" sort="Crossman, A R" uniqKey="Crossman A" first="A R" last="Crossman">A R Crossman</name><name sortKey="Gunne, L M" sort="Gunne, L M" uniqKey="Gunne L" first="L M" last="Gunne">L M Gunne</name><name sortKey="Liminga, U" sort="Liminga, U" uniqKey="Liminga U" first="U" last="Liminga">U. Liminga</name></noCountry><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></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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