Dopamine overdose hypothesis: evidence and clinical implications.
Identifieur interne : 000749 ( PubMed/Curation ); précédent : 000748; suivant : 000750Dopamine overdose hypothesis: evidence and clinical implications.
Auteurs : David E. Vaillancourt [États-Unis] ; Daniel Schonfeld ; Youngbin Kwak ; Nicolaas I. Bohnen ; Rachael SeidlerSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Brain (drug effects), Brain (metabolism), Cognition Disorders (drug therapy), Cognition Disorders (etiology), Dopamine (metabolism), Dopamine Agents (adverse effects), Humans, Learning Disorders (drug therapy), Learning Disorders (etiology), Levodopa (adverse effects), Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson Disease (pathology).
- MESH :
- chemical , adverse effects : Dopamine Agents, Levodopa.
- chemical , metabolism : Dopamine.
- complications : Parkinson Disease.
- drug effects : Brain.
- drug therapy : Cognition Disorders, Learning Disorders, Parkinson Disease.
- etiology : Cognition Disorders, Learning Disorders.
- metabolism : Brain.
- pathology : Parkinson Disease.
- Humans.
Abstract
About a half a century has passed since dopamine was identified as a neurotransmitter, and it has been several decades since it was established that people with Parkinson's disease receive motor symptom relief from oral levodopa. Despite the evidence that levodopa can reduce motor symptoms, there has been a developing body of literature that dopaminergic therapy can improve cognitive functions in some patients but make them worse in others. Over the past two decades, several laboratories have shown that dopaminergic medications can impair the action of intact neural structures and impair the behaviors associated with these structures. In this review, we consider the evidence that has accumulated in the areas of reversal learning, motor sequence learning, and other cognitive tasks. The purported inverted-U shaped relationship between dopamine levels and performance is complex and includes many contributory factors. The regional striatal topography of nigrostriatal denervation is a critical factor, as supported by multimodal neuroimaging studies. A patient's individual genotype will determine the relative baseline position on this inverted-U curve. Dopaminergic pharmacotherapy and individual gene polymorphisms can affect the mesolimbic and prefrontal cortical dopaminergic functions in a comparable, inverted-U dose-response relationship. Depending on these factors, a patient can respond positively or negatively to levodopa when performing reversal learning and motor sequence learning tasks. These tasks may continue to be relevant as our society moves to increased technological demands of a digital world that requires newly learned motor sequences and adaptive behaviors to manage daily life activities.
DOI: 10.1002/mds.25687
PubMed: 24123087
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Vaillancourt</name><affiliation wicri:level="1"><nlm:affiliation>Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA; Department of Neurology, University of Florida, Gainesville, Florida, USA; Department of Biomedical Engineering, University of Florida, Gainesville, Florida, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA; Department of Neurology, University of Florida, Gainesville, Florida, USA; Department of Biomedical Engineering, University of Florida, Gainesville, Florida</wicri:regionArea></affiliation></author><author><name sortKey="Schonfeld, Daniel" sort="Schonfeld, Daniel" uniqKey="Schonfeld D" first="Daniel" last="Schonfeld">Daniel Schonfeld</name></author><author><name sortKey="Kwak, Youngbin" sort="Kwak, Youngbin" uniqKey="Kwak Y" first="Youngbin" last="Kwak">Youngbin Kwak</name></author><author><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I" last="Bohnen">Nicolaas I. Bohnen</name></author><author><name sortKey="Seidler, Rachael" sort="Seidler, Rachael" uniqKey="Seidler R" first="Rachael" last="Seidler">Rachael Seidler</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:24123087</idno><idno type="pmid">24123087</idno><idno type="doi">10.1002/mds.25687</idno><idno type="wicri:Area/PubMed/Corpus">000749</idno><idno type="wicri:Area/PubMed/Curation">000749</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dopamine overdose hypothesis: evidence and clinical implications.</title><author><name sortKey="Vaillancourt, David E" sort="Vaillancourt, David E" uniqKey="Vaillancourt D" first="David E" last="Vaillancourt">David E. Vaillancourt</name><affiliation wicri:level="1"><nlm:affiliation>Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA; Department of Neurology, University of Florida, Gainesville, Florida, USA; Department of Biomedical Engineering, University of Florida, Gainesville, Florida, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA; Department of Neurology, University of Florida, Gainesville, Florida, USA; Department of Biomedical Engineering, University of Florida, Gainesville, Florida</wicri:regionArea></affiliation></author><author><name sortKey="Schonfeld, Daniel" sort="Schonfeld, Daniel" uniqKey="Schonfeld D" first="Daniel" last="Schonfeld">Daniel Schonfeld</name></author><author><name sortKey="Kwak, Youngbin" sort="Kwak, Youngbin" uniqKey="Kwak Y" first="Youngbin" last="Kwak">Youngbin Kwak</name></author><author><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I" last="Bohnen">Nicolaas I. Bohnen</name></author><author><name sortKey="Seidler, Rachael" sort="Seidler, Rachael" uniqKey="Seidler R" first="Rachael" last="Seidler">Rachael Seidler</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain (drug effects)</term><term>Brain (metabolism)</term><term>Cognition Disorders (drug therapy)</term><term>Cognition Disorders (etiology)</term><term>Dopamine (metabolism)</term><term>Dopamine Agents (adverse effects)</term><term>Humans</term><term>Learning Disorders (drug therapy)</term><term>Learning Disorders (etiology)</term><term>Levodopa (adverse effects)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Dopamine Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Cognition Disorders</term><term>Learning Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term><term>Learning Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">About a half a century has passed since dopamine was identified as a neurotransmitter, and it has been several decades since it was established that people with Parkinson's disease receive motor symptom relief from oral levodopa. Despite the evidence that levodopa can reduce motor symptoms, there has been a developing body of literature that dopaminergic therapy can improve cognitive functions in some patients but make them worse in others. Over the past two decades, several laboratories have shown that dopaminergic medications can impair the action of intact neural structures and impair the behaviors associated with these structures. In this review, we consider the evidence that has accumulated in the areas of reversal learning, motor sequence learning, and other cognitive tasks. The purported inverted-U shaped relationship between dopamine levels and performance is complex and includes many contributory factors. The regional striatal topography of nigrostriatal denervation is a critical factor, as supported by multimodal neuroimaging studies. A patient's individual genotype will determine the relative baseline position on this inverted-U curve. Dopaminergic pharmacotherapy and individual gene polymorphisms can affect the mesolimbic and prefrontal cortical dopaminergic functions in a comparable, inverted-U dose-response relationship. Depending on these factors, a patient can respond positively or negatively to levodopa when performing reversal learning and motor sequence learning tasks. These tasks may continue to be relevant as our society moves to increased technological demands of a digital world that requires newly learned motor sequences and adaptive behaviors to manage daily life activities.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">24123087</PMID><DateCreated><Year>2013</Year><Month>12</Month><Day>10</Day></DateCreated><DateCompleted><Year>2014</Year><Month>07</Month><Day>29</Day></DateCompleted><DateRevised><Year>2014</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>14</Issue><PubDate><Year>2013</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Dopamine overdose hypothesis: evidence and clinical implications.</ArticleTitle><Pagination><MedlinePgn>1920-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25687</ELocationID><Abstract><AbstractText>About a half a century has passed since dopamine was identified as a neurotransmitter, and it has been several decades since it was established that people with Parkinson's disease receive motor symptom relief from oral levodopa. Despite the evidence that levodopa can reduce motor symptoms, there has been a developing body of literature that dopaminergic therapy can improve cognitive functions in some patients but make them worse in others. Over the past two decades, several laboratories have shown that dopaminergic medications can impair the action of intact neural structures and impair the behaviors associated with these structures. In this review, we consider the evidence that has accumulated in the areas of reversal learning, motor sequence learning, and other cognitive tasks. The purported inverted-U shaped relationship between dopamine levels and performance is complex and includes many contributory factors. The regional striatal topography of nigrostriatal denervation is a critical factor, as supported by multimodal neuroimaging studies. A patient's individual genotype will determine the relative baseline position on this inverted-U curve. Dopaminergic pharmacotherapy and individual gene polymorphisms can affect the mesolimbic and prefrontal cortical dopaminergic functions in a comparable, inverted-U dose-response relationship. Depending on these factors, a patient can respond positively or negatively to levodopa when performing reversal learning and motor sequence learning tasks. These tasks may continue to be relevant as our society moves to increased technological demands of a digital world that requires newly learned motor sequences and adaptive behaviors to manage daily life activities.</AbstractText><CopyrightInformation>© 2013 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Vaillancourt</LastName><ForeName>David E</ForeName><Initials>DE</Initials><AffiliationInfo><Affiliation>Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA; Department of Neurology, University of Florida, Gainesville, Florida, USA; Department of Biomedical Engineering, University of Florida, Gainesville, Florida, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schonfeld</LastName><ForeName>Daniel</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Kwak</LastName><ForeName>Youngbin</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Bohnen</LastName><ForeName>Nicolaas I</ForeName><Initials>NI</Initials></Author><Author ValidYN="Y"><LastName>Seidler</LastName><ForeName>Rachael</ForeName><Initials>R</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 NS015655</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 NS015655</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS052318</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS052318</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS070856</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS070856</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS075012</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS075012</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>10</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>United 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MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015259">Dopamine Agents</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007859">Learning Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000009">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000188">drug 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PubStatus="entrez"><Year>2013</Year><Month>10</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>10</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>7</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24123087</ArticleId><ArticleId IdType="doi">10.1002/mds.25687</ArticleId><ArticleId IdType="pmc">PMC3859825</ArticleId><ArticleId IdType="mid">NIHMS521970</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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