Dopamine overdose hypothesis: Evidence and clinical implications
Identifieur interne : 000A19 ( Main/Exploration ); précédent : 000A18; suivant : 000A20Dopamine overdose hypothesis: Evidence and clinical implications
Auteurs : David E. Vaillancourt [États-Unis] ; Daniel Schonfeld [États-Unis] ; Youngbin Kwak [États-Unis] ; Nicolaas I. Bohnen [États-Unis] ; Rachael Seidler [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 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.
Url:
DOI: 10.1002/mds.25687
PubMed: 24123087
PubMed Central: 3859825
Affiliations:
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Bohnen</name><affiliation><nlm:aff id="A5">Neurology Service and GRECC, VA Ann Arbor Healthcare system</nlm:aff><wicri:noCountry code="subfield">VA Ann Arbor Healthcare system</wicri:noCountry></affiliation><affiliation wicri:level="2"><nlm:aff id="A6">Department of Neurology, University of Michigan, Ann Arbor, MI, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Michigan, Ann Arbor, MI</wicri:regionArea><placeName><region type="state">Michigan</region></placeName></affiliation><affiliation wicri:level="2"><nlm:aff id="A7">Department of Radiology, University of Michigan, Ann Arbor, MI, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Radiology, University of Michigan, Ann Arbor, MI</wicri:regionArea><placeName><region type="state">Michigan</region></placeName></affiliation></author><author><name sortKey="Seidler, Rachael" sort="Seidler, Rachael" uniqKey="Seidler R" first="Rachael" last="Seidler">Rachael Seidler</name><affiliation wicri:level="2"><nlm:aff id="A8">Department of Neuroscience, University of Michigan, Ann Arbor, MI, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neuroscience, University of Michigan, Ann Arbor, MI</wicri:regionArea><placeName><region type="state">Michigan</region></placeName></affiliation><affiliation wicri:level="2"><nlm:aff id="A9">Department of Psychology, University of Michigan, Ann Arbor, MI, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Psychology, University of Michigan, Ann Arbor, MI</wicri:regionArea><placeName><region type="state">Michigan</region></placeName></affiliation><affiliation wicri:level="2"><nlm:aff id="A10">School of Kinesiology, University of Michigan, Ann Arbor, MI, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>School of Kinesiology, University of Michigan, Ann Arbor, MI</wicri:regionArea><placeName><region type="state">Michigan</region></placeName></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2013">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"><title>Summary</title><p id="P1">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.</p></div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Caroline du Nord</li><li>Floride</li><li>Michigan</li></region></list><tree><country name="États-Unis"><region name="Floride"><name sortKey="Vaillancourt, David E" sort="Vaillancourt, David E" uniqKey="Vaillancourt D" first="David E." last="Vaillancourt">David E. Vaillancourt</name></region><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I." last="Bohnen">Nicolaas I. Bohnen</name><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I." last="Bohnen">Nicolaas I. Bohnen</name><name sortKey="Kwak, Youngbin" sort="Kwak, Youngbin" uniqKey="Kwak Y" first="Youngbin" last="Kwak">Youngbin Kwak</name><name sortKey="Schonfeld, Daniel" sort="Schonfeld, Daniel" uniqKey="Schonfeld D" first="Daniel" last="Schonfeld">Daniel Schonfeld</name><name sortKey="Seidler, Rachael" sort="Seidler, Rachael" uniqKey="Seidler R" first="Rachael" last="Seidler">Rachael Seidler</name><name sortKey="Seidler, Rachael" sort="Seidler, Rachael" uniqKey="Seidler R" first="Rachael" last="Seidler">Rachael Seidler</name><name sortKey="Seidler, Rachael" sort="Seidler, Rachael" uniqKey="Seidler R" first="Rachael" last="Seidler">Rachael Seidler</name><name sortKey="Vaillancourt, David E" sort="Vaillancourt, David E" uniqKey="Vaillancourt D" first="David E." last="Vaillancourt">David E. Vaillancourt</name><name sortKey="Vaillancourt, David E" sort="Vaillancourt, David E" uniqKey="Vaillancourt D" first="David E." last="Vaillancourt">David E. Vaillancourt</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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