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Dopamine-receptor stimulation: biobehavioral and biochemical consequences

Identifieur interne : 002681 ( Istex/Corpus ); précédent : 002680; suivant : 002682

Dopamine-receptor stimulation: biobehavioral and biochemical consequences

Auteurs : Frédéric Calon ; Abdallah Hadj Tahar ; Pierre J. Blanchet ; Marc Morissette ; Richard Grondin ; Martin Goulet ; Jean-Pierre Doucet ; George S. Robertson ; Eric Nestler ; Thérèse Di Paolo ; Paul J. Bédard

Source :

RBID : ISTEX:F5021E916FA1644FC98FFA3C109970BDE219090A

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

Links to Exploration step

ISTEX:F5021E916FA1644FC98FFA3C109970BDE219090A

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<forename type="first">Richard</forename>
<surname>Grondin</surname>
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<affiliation>Oncology and Molecular Endocrinology Research Unit, Laval University Medical Center (CHUL), Québec, Canada GIV 4G2</affiliation>
<affiliation>Faculty of Pharmacy, Laval University, Québec, Canada GIK 7P4</affiliation>
<affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, Canada G1V 4G2</affiliation>
<affiliation>Dept of Medicine, Faculty of Medicine, Laval University, Québec, Canada GIK 7P4</affiliation>
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<persName>
<forename type="first">Martin</forename>
<surname>Goulet</surname>
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<affiliation>Oncology and Molecular Endocrinology Research Unit, Laval University Medical Center (CHUL), Québec, Canada GIV 4G2</affiliation>
<affiliation>Faculty of Pharmacy, Laval University, Québec, Canada GIK 7P4</affiliation>
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<persName>
<forename type="first">Jean-Pierre</forename>
<surname>Doucet</surname>
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<affiliation>Dept of Pharmacology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada</affiliation>
</author>
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<persName>
<forename type="first">George S.</forename>
<surname>Robertson</surname>
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<affiliation>Dept of Pharmacology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada</affiliation>
</author>
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<persName>
<forename type="first">Eric</forename>
<surname>Nestler</surname>
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<affiliation>Oncology and Molecular Endocrinology Research Unit, Laval University Medical Center (CHUL), Québec, Canada GIV 4G2</affiliation>
<affiliation>Faculty of Pharmacy, Laval University, Québec, Canada GIK 7P4</affiliation>
</author>
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<persName>
<forename type="first">Paul J.</forename>
<surname>Bédard</surname>
</persName>
<affiliation>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, Canada G1V 4G2</affiliation>
<affiliation>Dept of Medicine, Faculty of Medicine, Laval University, Québec, Canada GIK 7P4</affiliation>
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<p>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.</p>
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<ce:doi>10.1016/S1471-1931(00)00026-4</ce:doi>
<ce:copyright type="unknown" year="2000">Elsevier Science Ltd. All rights reserved.</ce:copyright>
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<head>
<ce:dochead>
<ce:textfn>Review</ce:textfn>
</ce:dochead>
<ce:title>Dopamine-receptor stimulation: biobehavioral and biochemical consequences</ce:title>
<ce:author-group>
<ce:author>
<ce:given-name>Frédéric</ce:given-name>
<ce:surname>Calon</ce:surname>
<ce:cross-ref refid="aff1">
<ce:sup>a</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff2">
<ce:sup>b</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>Abdallah Hadj</ce:given-name>
<ce:surname>Tahar</ce:surname>
<ce:cross-ref refid="aff3">
<ce:sup>c</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff4">
<ce:sup>d</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>Pierre J.</ce:given-name>
<ce:surname>Blanchet</ce:surname>
<ce:cross-ref refid="aff3">
<ce:sup>c</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff4">
<ce:sup>d</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>Marc</ce:given-name>
<ce:surname>Morissette</ce:surname>
<ce:cross-ref refid="aff1">
<ce:sup>a</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff2">
<ce:sup>b</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>Richard</ce:given-name>
<ce:surname>Grondin</ce:surname>
<ce:cross-ref refid="aff1">
<ce:sup>a</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff2">
<ce:sup>b</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff3">
<ce:sup>c</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff4">
<ce:sup>d</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>Martin</ce:given-name>
<ce:surname>Goulet</ce:surname>
<ce:cross-ref refid="aff1">
<ce:sup>a</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff2">
<ce:sup>b</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>Jean-Pierre</ce:given-name>
<ce:surname>Doucet</ce:surname>
<ce:cross-ref refid="aff5">
<ce:sup>e</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>George S.</ce:given-name>
<ce:surname>Robertson</ce:surname>
<ce:cross-ref refid="aff5">
<ce:sup>e</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>Eric</ce:given-name>
<ce:surname>Nestler</ce:surname>
<ce:cross-ref refid="aff6">
<ce:sup>f</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>Thérèse</ce:given-name>
<ce:surname>Di Paolo</ce:surname>
<ce:cross-ref refid="aff1">
<ce:sup>a</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff2">
<ce:sup>b</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:author>
<ce:given-name>Paul J.</ce:given-name>
<ce:surname>Bédard</ce:surname>
<ce:cross-ref refid="aff3">
<ce:sup>c</ce:sup>
</ce:cross-ref>
<ce:cross-ref refid="aff4">
<ce:sup>d</ce:sup>
</ce:cross-ref>
</ce:author>
<ce:affiliation id="aff1">
<ce:label>a</ce:label>
<ce:textfn>Oncology and Molecular Endocrinology Research Unit, Laval University Medical Center (CHUL), Québec, Canada GIV 4G2</ce:textfn>
</ce:affiliation>
<ce:affiliation id="aff2">
<ce:label>b</ce:label>
<ce:textfn>Faculty of Pharmacy, Laval University, Québec, Canada GIK 7P4</ce:textfn>
</ce:affiliation>
<ce:affiliation id="aff3">
<ce:label>c</ce:label>
<ce:textfn>Neuroscience Research Unit, Laval University Medical Center (CHUL), Québec, Canada G1V 4G2</ce:textfn>
</ce:affiliation>
<ce:affiliation id="aff4">
<ce:label>d</ce:label>
<ce:textfn>Dept of Medicine, Faculty of Medicine, Laval University, Québec, Canada GIK 7P4</ce:textfn>
</ce:affiliation>
<ce:affiliation id="aff5">
<ce:label>e</ce:label>
<ce:textfn>Dept of Pharmacology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada</ce:textfn>
</ce:affiliation>
<ce:affiliation id="aff6">
<ce:label>f</ce:label>
<ce:textfn>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, USA</ce:textfn>
</ce:affiliation>
</ce:author-group>
<ce:abstract id="ab1" class="author" xml:lang="en">
<ce:abstract-sec>
<ce:simple-para>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
<ce:small-caps>l</ce:small-caps>
-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.</ce:simple-para>
</ce:abstract-sec>
</ce:abstract>
</head>
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<abstract 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.</abstract>
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