ParkinsonCanadaV1, PascalFrancis, Curation, bibRecord, 000622

Dopamine dysregulation syndrome : implications for a dopamine hypothesis of bipolar disorder

Identifieur interne : 000622 ( PascalFrancis/Curation ); précédent : 000621; suivant : 000623

Dopamine dysregulation syndrome : implications for a dopamine hypothesis of bipolar disorder

Auteurs : M. Berk [Australie] ; S. Dodd [Australie] ; M. Kauer-Sant'Anna [Canada] ; G. S. Malhi [Australie] ; M. Bourin [France] ; F. Kapczinski [Brésil] ; T. Norman [Australie]

Source :

Acta psychiatrica scandinavica. Supplementum [ 0065-1591 ] ; 2007.

RBID : Pascal:08-0007460

Descripteurs français

Pascal (Inist)
- Dopamine, Trouble bipolaire, Manie, Etat dépressif, Physiopathologie, Transmission dopaminergique, Psychopharmacologie, Article synthèse, Homme.
Wicri :
- topic : Homme.

English descriptors

KwdEn :
- Bipolar disorder, Depression, Dopamine, Dopaminergic transmission, Human, Mania, Pathophysiology, Psychopharmacology, Review.

Abstract

Objective: Rational therapeutic development in bipolar is hampered by a lack of pathophysiological model. However, there is a wealth of converging data on the role of dopamine in bipolar disorder. This paper therefore examines the possibility of a dopamine hypothesis for bipolar disorder. Method: A literature search was conducted using standard search engines Embase, PyschLIT, PubMed and MEDLINE. In addition, papers and book chapters known to the authors were retrieved and examined for further relevant articles. Results: Collectively, in excess of 100 articles were reviewed from which approximately 75% were relevant to the focus of this paper. Conclusion: Pharmacological models suggest a role of increased dopaminergic drive in mania and the converse in depression. In Parkinson's disease, administration of high-dose dopamine precursors can produce a 'maniform' picture, which switches into a depressive analogue on withdrawal. It is possible that in bipolar disorder there is a cyclical process, where increased dopaminergic transmission in mania leads to a secondary down regulation of dopaminergic receptor sensitivity over time. This may lead to a period of decreased dopaminergic transmission, corresponding with the depressive phase, and the repetition of the cycle. This model, if verified, may have implications for rational drug development.

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C01	`01`		`ENG`	@0 Objective: Rational therapeutic development in bipolar is hampered by a lack of pathophysiological model. However, there is a wealth of converging data on the role of dopamine in bipolar disorder. This paper therefore examines the possibility of a dopamine hypothesis for bipolar disorder. Method: A literature search was conducted using standard search engines Embase, PyschLIT, PubMed and MEDLINE. In addition, papers and book chapters known to the authors were retrieved and examined for further relevant articles. Results: Collectively, in excess of 100 articles were reviewed from which approximately 75% were relevant to the focus of this paper. Conclusion: Pharmacological models suggest a role of increased dopaminergic drive in mania and the converse in depression. In Parkinson's disease, administration of high-dose dopamine precursors can produce a 'maniform' picture, which switches into a depressive analogue on withdrawal. It is possible that in bipolar disorder there is a cyclical process, where increased dopaminergic transmission in mania leads to a secondary down regulation of dopaminergic receptor sensitivity over time. This may lead to a period of decreased dopaminergic transmission, corresponding with the depressive phase, and the repetition of the cycle. This model, if verified, may have implications for rational drug development.
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C03	`01`	`X`	`SPA`	`@0 Dopamina @2 NK @2 FR @5 01`
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C03	`05`	`X`	`ENG`	`@0 Pathophysiology @5 05`
C03	`05`	`X`	`SPA`	`@0 Fisiopatología @5 05`
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C03	`09`	`X`	`FRE`	`@0 Homme @5 18`
C03	`09`	`X`	`ENG`	`@0 Human @5 18`
C03	`09`	`X`	`SPA`	`@0 Hombre @5 18`
C07	`01`	`X`	`FRE`	`@0 Catécholamine @5 37`
C07	`01`	`X`	`ENG`	`@0 Catecholamine @5 37`
C07	`01`	`X`	`SPA`	`@0 Catecolamina @5 37`
C07	`02`	`X`	`FRE`	`@0 Neurotransmetteur @5 38`
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Links toward previous steps (curation, corpus...)

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Pascal:08-0007460

Le document en format XML

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<front><div type="abstract" xml:lang="en">Objective: Rational therapeutic development in bipolar is hampered by a lack of pathophysiological model. However, there is a wealth of converging data on the role of dopamine in bipolar disorder. This paper therefore examines the possibility of a dopamine hypothesis for bipolar disorder. Method: A literature search was conducted using standard search engines Embase, PyschLIT, PubMed and MEDLINE. In addition, papers and book chapters known to the authors were retrieved and examined for further relevant articles. Results: Collectively, in excess of 100 articles were reviewed from which approximately 75% were relevant to the focus of this paper. Conclusion: Pharmacological models suggest a role of increased dopaminergic drive in mania and the converse in depression. In Parkinson's disease, administration of high-dose dopamine precursors can produce a 'maniform' picture, which switches into a depressive analogue on withdrawal. It is possible that in bipolar disorder there is a cyclical process, where increased dopaminergic transmission in mania leads to a secondary down regulation of dopaminergic receptor sensitivity over time. This may lead to a period of decreased dopaminergic transmission, corresponding with the depressive phase, and the repetition of the cycle. This model, if verified, may have implications for rational drug development.</div>
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<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>CADE Clinic, Department of Psychiatry, Royal North Shore Hospital</s1>
<s2>Sydney, NSW</s2>
<s3>AUS</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Université de Nantes, EA 3256 -Neurobiologie de l'Anxiété et de la Dépression</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Laboratório de Psiquiatria Molecular, Centro de Pesquisas, Hospital de Clínicas de Porto Alegre</s1>
<s2>Porto Alegre, RS</s2>
<s3>BRA</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="09"><s1>Department of Psychiatry, University of Melbourne</s1>
<s2>Melbourne, Vic</s2>
<s3>AUS</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA15 i1="01"><s1>Department of Psychological Medicine, Northern Clinical School, University of Sydney</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
</fA15>
<fA15 i1="02"><s1>CADE Clinic, Royal North Shore Hospital</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
</fA15>
<fA15 i1="03"><s1>Mood Disorders Unit, Black Dog Institute, Prince of Wales Hospital</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
</fA15>
<fA15 i1="04"><s1>Mood Disorders Clinical Research Unit, The University of British Columbia</s1>
<s2>Vancouver, BC</s2>
<s3>CAN</s3>
<sZ>2 aut.</sZ>
</fA15>
<fA20><s1>41-49</s1>
</fA20>
<fA21><s1>2007</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>3204B</s2>
<s5>354000149752300050</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2008 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>77 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>08-0007460</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Acta psychiatrica scandinavica. Supplementum</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Objective: Rational therapeutic development in bipolar is hampered by a lack of pathophysiological model. However, there is a wealth of converging data on the role of dopamine in bipolar disorder. This paper therefore examines the possibility of a dopamine hypothesis for bipolar disorder. Method: A literature search was conducted using standard search engines Embase, PyschLIT, PubMed and MEDLINE. In addition, papers and book chapters known to the authors were retrieved and examined for further relevant articles. Results: Collectively, in excess of 100 articles were reviewed from which approximately 75% were relevant to the focus of this paper. Conclusion: Pharmacological models suggest a role of increased dopaminergic drive in mania and the converse in depression. In Parkinson's disease, administration of high-dose dopamine precursors can produce a 'maniform' picture, which switches into a depressive analogue on withdrawal. It is possible that in bipolar disorder there is a cyclical process, where increased dopaminergic transmission in mania leads to a secondary down regulation of dopaminergic receptor sensitivity over time. This may lead to a period of decreased dopaminergic transmission, corresponding with the depressive phase, and the repetition of the cycle. This model, if verified, may have implications for rational drug development.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B18C07C</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Dopamine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Dopamina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Trouble bipolaire</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Bipolar disorder</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Trastorno bipolar</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Manie</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Mania</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Mania</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Etat dépressif</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Depression</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Estado depresivo</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Physiopathologie</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Pathophysiology</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Fisiopatología</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Transmission dopaminergique</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Dopaminergic transmission</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Transmisión dopaminérgica</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Psychopharmacologie</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Psychopharmacology</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Psicofarmacología</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Article synthèse</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Review</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Artículo síntesis</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Homme</s0>
<s5>18</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Human</s0>
<s5>18</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Hombre</s0>
<s5>18</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Trouble de l'humeur</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Mood disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Trastorno humor</s0>
<s5>39</s5>
</fC07>
<fN21><s1>007</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Dopamine dysregulation syndrome : implications for a dopamine hypothesis of bipolar disorder

Dopamine dysregulation syndrome : implications for a dopamine hypothesis of bipolar disorder

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