Dopamine-receptor stimulation : biobehavioral and biochemical consequences
Identifieur interne : 000076 ( PascalFrancis/Curation ); précédent : 000075; suivant : 000077Dopamine-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. Bedard [Canada]Source :
- Trends in neurosciences : (Regular edition) [ 0166-2236 ] ; 2000.
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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 (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.
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Dopamine-receptor stimulation : biobehavioral and biochemical consequences</title>
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<affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Dept of Medicine, Faculty of Medicine, Laval University</s1>
<s2>Québec, G1K 7P4</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>11 aut.</sZ>
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<series><title level="j" type="main">Trends in neurosciences : (Regular edition)</title>
<title level="j" type="abbreviated">Trends neurosci. : (Regul. ed.)</title>
<idno type="ISSN">0166-2236</idno>
<imprint><date when="2000">2000</date>
</imprint>
</series>
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</sourceDesc>
<seriesStmt><title level="j" type="main">Trends in neurosciences : (Regular edition)</title>
<title level="j" type="abbreviated">Trends neurosci. : (Regul. ed.)</title>
<idno type="ISSN">0166-2236</idno>
</seriesStmt>
</fileDesc>
<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>
<term>Review</term>
</keywords>
<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>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term>
</keywords>
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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>
</front>
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<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0166-2236</s0>
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<fA03 i2="1"><s0>Trends neurosci. : (Regul. ed.)</s0>
</fA03>
<fA05><s2>23</s2>
</fA05>
<fA06><s2>10</s2>
<s3>SUP</s3>
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<fA08 i1="01" i2="1" l="ENG"><s1>Dopamine-receptor stimulation : biobehavioral and biochemical consequences</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>CALON (Frédéric)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>ABDALLAH HADJ TAHAR</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>BLANCHET (Pierre J.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>MORISSETTE (Marc)</s1>
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<fA11 i1="05" i2="1"><s1>GRONDIN (Richard)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>GOULET (Martin)</s1>
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<fA11 i1="07" i2="1"><s1>DOUCET (Jean-Pierre)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>ROBERTSON (George S.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>NESTLER (Eric)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>DI PAOLO (Thérèse)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>BEDARD (Paul J.)</s1>
</fA11>
<fA14 i1="01"><s1>Oncology and Molecular Endocrinology Research Unit, Laval University Medical Center (CHUL)</s1>
<s2>Québec, G1V 4G2</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Faculty of Pharmacy, Laval University</s1>
<s2>Québec, G1K 7P4</s2>
<s3>CAN</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Neuroscience Research Unit, Laval University Medical Center (CHUL)</s1>
<s2>Québec, G1V 4G2</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>11 aut.</sZ>
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<fA14 i1="04"><s1>Dept of Medicine, Faculty of Medicine, Laval University</s1>
<s2>Québec, G1K 7P4</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Dept of Pharmacology, Faculty of Medicine, University of Ottawa</s1>
<s2>Ottawa, Ontario</s2>
<s3>CAN</s3>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Laboratory of Molecular Psychiatry and Yale Center for Genes and Behavior, Yale University School of Medicine and Connecticut Mental Health Center</s1>
<s2>New Haven, CT 06508</s2>
<s3>USA</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA20><s2>S92-S100</s2>
</fA20>
<fA21><s1>2000</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
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<fA43 i1="01"><s1>INIST</s1>
<s2>18018B</s2>
<s5>354000092959410120</s5>
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<fA44><s0>0000</s0>
<s1>© 2001 INIST-CNRS. All rights reserved.</s1>
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<fA45><s0>86 ref.</s0>
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<fA47 i1="01" i2="1"><s0>01-0111009</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Trends in neurosciences : (Regular edition)</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>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.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Article synthèse</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Review</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Artículo síntesis</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Parkinsonisme</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Parkinsonism</s0>
<s2>NM</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Parkinson síndrome</s0>
<s2>NM</s2>
<s5>02</s5>
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<fC03 i1="03" i2="X" l="FRE"><s0>Récepteur dopaminergique</s0>
<s5>03</s5>
</fC03>
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<s5>03</s5>
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<fC03 i1="03" i2="X" l="SPA"><s0>Receptor dopaminérgico</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Dyskinésie</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Dyskinesia</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Disquinesia</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Lévodopa</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Levodopa</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Levodopa</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Expression génique</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Gene expression</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Expresión genética</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Transmission gabaergique</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Gabaergic transmission</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Transmisión gabaérgica</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Transmission glutamatergique</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Glutamatergic transmission</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Transmision glutamatérgica</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Noyau gris central</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Basal ganglion</s0>
<s5>10</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Núcleo basal</s0>
<s5>10</s5>
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<fC03 i1="10" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Singe</s0>
<s5>54</s5>
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<fC03 i1="11" i2="X" l="ENG"><s0>Monkey</s0>
<s5>54</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Mono</s0>
<s5>54</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>45</s5>
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<fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>45</s5>
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<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>45</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>46</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>46</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>46</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>47</s5>
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<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>47</s5>
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<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>47</s5>
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<s5>48</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>48</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>48</s5>
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<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>49</s5>
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<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>49</s5>
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<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>49</s5>
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<fC07 i1="06" i2="X" l="FRE"><s0>Primates</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Primates</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Primates</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>071</s1>
</fN21>
</pA>
</standard>
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