Dopamine-receptor stimulation: biobehavioral and biochemical consequences
Identifieur interne : 003512 ( Main/Curation ); précédent : 003511; suivant : 003513Dopamine-receptor stimulation: biobehavioral and biochemical consequences
Auteurs : Frédéric Calon [Canada] ; Abdallah Hadj Tahar [Canada] ; Pierre J. Blanchet [Canada] ; Marc Morissette [Canada] ; Richard Grondin [Canada] ; Martin Goulet [Canada] ; Jean-Pierre Doucet [Canada] ; George S. Robertson [Canada] ; Eric Nestler [États-Unis] ; Thérèse Di Paolo [Canada] ; Paul J. Bédard [Canada]Source :
- Trends in Neurosciences [ 0166-2236 ] ; 2000.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
Abstract
The MPTP monkey is a well-characterized animal model of parkinsonism and provides an exceptional tool for the study of dyskinesias induced by dopamine-like agents. Several such agents have been tested during the past 15 years, and it has been found that the duration of action of these compounds is the most reliable variable with which to predict their dyskinesiogenic profile. It is proposed that l-dopa-induced dyskinesias represent a form of pathological learning caused by chronic pulsatile (non physiological) stimulation of dopamine receptors, which activates a cascade of molecular and biochemical events. These events include defective regulation of Fos proteins that belong to the ΔFosB family, increased expression of neuropeptides, and defective GABA- and glutamate-mediated neurotransmission in the output structures of the basal ganglia.
Url:
DOI: 10.1016/S1471-1931(00)00026-4
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<front><div type="abstract" xml:lang="en">The MPTP monkey is a well-characterized animal model of parkinsonism and provides an exceptional tool for the study of dyskinesias induced by dopamine-like agents. Several such agents have been tested during the past 15 years, and it has been found that the duration of action of these compounds is the most reliable variable with which to predict their dyskinesiogenic profile. It is proposed that l-dopa-induced dyskinesias represent a form of pathological learning caused by chronic pulsatile (non physiological) stimulation of dopamine receptors, which activates a cascade of molecular and biochemical events. These events include defective regulation of Fos proteins that belong to the ΔFosB family, increased expression of neuropeptides, and defective GABA- and glutamate-mediated neurotransmission in the output structures of the basal ganglia.</div>
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<series><title level="j" type="main">Trends in neurosciences : (Regular edition)</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basal ganglion</term>
<term>Dopamine receptor</term>
<term>Dyskinesia</term>
<term>Gabaergic transmission</term>
<term>Gene expression</term>
<term>Glutamatergic transmission</term>
<term>Levodopa</term>
<term>Monkey</term>
<term>Parkinson disease</term>
<term>Parkinsonism</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Article synthèse</term>
<term>Parkinsonisme</term>
<term>Récepteur dopaminergique</term>
<term>Dyskinésie</term>
<term>Lévodopa</term>
<term>Expression génique</term>
<term>Transmission gabaergique</term>
<term>Transmission glutamatergique</term>
<term>Noyau gris central</term>
<term>Parkinson maladie</term>
<term>Singe</term>
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<front><div type="abstract" xml:lang="en">The MPTP monkey is a well-characterized animal model of parkinsonism and provides an exceptional tool for the study of dyskinesias induced by dopamine-like agents. Several such agents have been tested during the past 15 years, and it has been found that the duration of action of these compounds is the most reliable variable with which to predict their dyskinesiogenic profile. It is proposed that L-dopa-induced dyskinesias represent a form of pathological learning caused by chronic pulsatile (nonphysiological) stimulation of dopamine receptors, which activates a cascade of molecular and biochemical events. These events include defective regulation of Fos proteins that belong to the ΔFosB family, increased expression of neuropeptides, and defective GABA- and glutamate-mediated neurotransmission in the output structures of the basal ganglia.</div>
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<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Faculty of Pharmacy, Laval University, Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Tahar, Abdallah Hadj" sort="Tahar, Abdallah Hadj" uniqKey="Tahar A" first="Abdallah Hadj" last="Tahar">Abdallah Hadj Tahar</name>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Dept of Medicine, Faculty of Medicine, Laval University, Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Blanchet, Pierre J" sort="Blanchet, Pierre J" uniqKey="Blanchet P" first="Pierre J." last="Blanchet">Pierre J. Blanchet</name>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Dept of Medicine, Faculty of Medicine, Laval University, Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Morissette, Marc" sort="Morissette, Marc" uniqKey="Morissette M" first="Marc" last="Morissette">Marc Morissette</name>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Oncology and Molecular Endocrinology Research Unit, Laval University Medical Center (CHUL), Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Faculty of Pharmacy, Laval University, Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Grondin, Richard" sort="Grondin, Richard" uniqKey="Grondin R" first="Richard" last="Grondin">Richard Grondin</name>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Oncology and Molecular Endocrinology Research Unit, Laval University Medical Center (CHUL), Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Faculty of Pharmacy, Laval University, Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Dept of Medicine, Faculty of Medicine, Laval University, Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Goulet, Martin" sort="Goulet, Martin" uniqKey="Goulet M" first="Martin" last="Goulet">Martin Goulet</name>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Oncology and Molecular Endocrinology Research Unit, Laval University Medical Center (CHUL), Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Faculty of Pharmacy, Laval University, Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Doucet, Jean Pierre" sort="Doucet, Jean Pierre" uniqKey="Doucet J" first="Jean-Pierre" last="Doucet">Jean-Pierre Doucet</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Dept of Pharmacology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Robertson, George S" sort="Robertson, George S" uniqKey="Robertson G" first="George S." last="Robertson">George S. Robertson</name>
<affiliation wicri:level="1"><country xml:lang="fr">Canada</country>
<wicri:regionArea>Dept of Pharmacology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario</wicri:regionArea>
<wicri:noRegion>Ontario</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Nestler, Eric" sort="Nestler, Eric" uniqKey="Nestler E" first="Eric" last="Nestler">Eric Nestler</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Laboratory of Molecular Psychiatry and Yale Center for Genes and Behavior, Yale University School of Medicine and Connecticut Mental Health Center, New Haven, CT 06508</wicri:regionArea>
<placeName><region type="state">Connecticut</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Oncology and Molecular Endocrinology Research Unit, Laval University Medical Center (CHUL), Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Faculty of Pharmacy, Laval University, Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Bedard, Paul J" sort="Bedard, Paul J" uniqKey="Bedard P" first="Paul J." last="Bédard">Paul J. Bédard</name>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country>Canada</country>
<wicri:regionArea>Dept of Medicine, Faculty of Medicine, Laval University, Québec</wicri:regionArea>
<wicri:noRegion>Québec</wicri:noRegion>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Trends in Neurosciences</title>
<title level="j" type="abbrev">TINS</title>
<idno type="ISSN">0166-2236</idno>
<imprint><publisher>ELSEVIER</publisher>
<date type="published" when="2000">2000</date>
<biblScope unit="volume">23</biblScope>
<biblScope unit="supplement">S1</biblScope>
<biblScope unit="page" from="S92">S92</biblScope>
<biblScope unit="page" to="S100">S100</biblScope>
</imprint>
<idno type="ISSN">0166-2236</idno>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0166-2236</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass></textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">The MPTP monkey is a well-characterized animal model of parkinsonism and provides an exceptional tool for the study of dyskinesias induced by dopamine-like agents. Several such agents have been tested during the past 15 years, and it has been found that the duration of action of these compounds is the most reliable variable with which to predict their dyskinesiogenic profile. It is proposed that l-dopa-induced dyskinesias represent a form of pathological learning caused by chronic pulsatile (non physiological) stimulation of dopamine receptors, which activates a cascade of molecular and biochemical events. These events include defective regulation of Fos proteins that belong to the ΔFosB family, increased expression of neuropeptides, and defective GABA- and glutamate-mediated neurotransmission in the output structures of the basal ganglia.</div>
</front>
</TEI>
</ISTEX>
</double>
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