Physiology of the normal and dopamine-depleted basal ganglia: insights into levodopa pharmacotherapy.
Identifieur interne : 002143 ( PubMed/Checkpoint ); précédent : 002142; suivant : 002144Physiology of the normal and dopamine-depleted basal ganglia: insights into levodopa pharmacotherapy.
Auteurs : Anthony A. Grace [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Antiparkinson Agents (therapeutic use), Basal Ganglia (drug effects), Basal Ganglia (physiology), Dopamine (deficiency), Dopamine (pharmacology), Dopamine (physiology), Humans, Levodopa (therapeutic use), Neurons (drug effects), Neurons (pathology), Neurons (physiology), Nucleus Accumbens (physiology), Parkinson Disease (drug therapy), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Receptors, Dopamine (drug effects), Receptors, Dopamine (physiology), Synapses (drug effects), Synapses (physiology), Synaptic Transmission (drug effects), Synaptic Transmission (physiology), gamma-Aminobutyric Acid (physiology).
- MESH :
- chemical , deficiency : Dopamine.
- chemical , drug effects : Receptors, Dopamine.
- chemical , pharmacology : Dopamine.
- chemical , physiology : Dopamine, Receptors, Dopamine, gamma-Aminobutyric Acid.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug effects : Basal Ganglia, Neurons, Synapses, Synaptic Transmission.
- drug therapy : Parkinson Disease.
- pathology : Neurons, Parkinson Disease.
- physiology : Basal Ganglia, Neurons, Nucleus Accumbens, Synapses, Synaptic Transmission.
- physiopathology : Parkinson Disease.
- Humans.
Abstract
Dopamine (DA) neurons exist in two activity states; either spontaneously firing or quiescent and nonfiring. When faced with a behavioral demand, the quiescent DA neurons can be activated to facilitate normal motor output. Levodopa appears to increase DA output by activating these nonfiring neurons; as a consequence, DA release is increased, but behavioral demand can now overwhelm the system, potentially leading to the inactivation and on/off phenomena. Levodopa administered in a pulsatile manner may also lead to the induction of synaptic plasticity within the DA systems. In the ventral mesolimbic system, this could lead to the loss of behavioral flexibility, impulsive behavior, and cognitive impairment, whereas in the dorsal nigrostriatal system, this may underlie Levodopa-induced dyskinesia. Continuous administration of Levodopa may circumvent this sensitization process, enabling a therapeutic response without limbic and motor side effects.
DOI: 10.1002/mds.22020
PubMed: 18781673
Affiliations:
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Graceaa@pitt.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neuroscience, Center for Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="doi">10.1002/mds.22020</idno><idno type="RBID">pubmed:18781673</idno><idno type="pmid">18781673</idno><idno type="wicri:Area/PubMed/Corpus">002057</idno><idno type="wicri:Area/PubMed/Curation">002057</idno><idno type="wicri:Area/PubMed/Checkpoint">002143</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Physiology of the normal and dopamine-depleted basal ganglia: insights into levodopa pharmacotherapy.</title><author><name sortKey="Grace, Anthony A" sort="Grace, Anthony A" uniqKey="Grace A" first="Anthony A" last="Grace">Anthony A. Grace</name><affiliation wicri:level="4"><nlm:affiliation>Department of Neuroscience, Center for Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. Graceaa@pitt.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neuroscience, Center for Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></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="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiparkinson Agents (therapeutic use)</term><term>Basal Ganglia (drug effects)</term><term>Basal Ganglia (physiology)</term><term>Dopamine (deficiency)</term><term>Dopamine (pharmacology)</term><term>Dopamine (physiology)</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Neurons (drug effects)</term><term>Neurons (pathology)</term><term>Neurons (physiology)</term><term>Nucleus Accumbens (physiology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Receptors, Dopamine (drug effects)</term><term>Receptors, Dopamine (physiology)</term><term>Synapses (drug effects)</term><term>Synapses (physiology)</term><term>Synaptic Transmission (drug effects)</term><term>Synaptic Transmission (physiology)</term><term>gamma-Aminobutyric Acid (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term><term>Receptors, Dopamine</term><term>gamma-Aminobutyric Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Basal Ganglia</term><term>Neurons</term><term>Synapses</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Basal Ganglia</term><term>Neurons</term><term>Nucleus Accumbens</term><term>Synapses</term><term>Synaptic Transmission</term></keywords><keywords scheme="MESH" qualifier="physiopathology" 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">Dopamine (DA) neurons exist in two activity states; either spontaneously firing or quiescent and nonfiring. When faced with a behavioral demand, the quiescent DA neurons can be activated to facilitate normal motor output. Levodopa appears to increase DA output by activating these nonfiring neurons; as a consequence, DA release is increased, but behavioral demand can now overwhelm the system, potentially leading to the inactivation and on/off phenomena. Levodopa administered in a pulsatile manner may also lead to the induction of synaptic plasticity within the DA systems. In the ventral mesolimbic system, this could lead to the loss of behavioral flexibility, impulsive behavior, and cognitive impairment, whereas in the dorsal nigrostriatal system, this may underlie Levodopa-induced dyskinesia. Continuous administration of Levodopa may circumvent this sensitization process, enabling a therapeutic response without limbic and motor side effects.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">18781673</PMID><DateCreated><Year>2008</Year><Month>09</Month><Day>18</Day></DateCreated><DateCompleted><Year>2009</Year><Month>02</Month><Day>13</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23 Suppl 3</Volume><PubDate><Year>2008</Year></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Physiology of the normal and dopamine-depleted basal ganglia: insights into levodopa pharmacotherapy.</ArticleTitle><Pagination><MedlinePgn>S560-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22020</ELocationID><Abstract><AbstractText>Dopamine (DA) neurons exist in two activity states; either spontaneously firing or quiescent and nonfiring. When faced with a behavioral demand, the quiescent DA neurons can be activated to facilitate normal motor output. Levodopa appears to increase DA output by activating these nonfiring neurons; as a consequence, DA release is increased, but behavioral demand can now overwhelm the system, potentially leading to the inactivation and on/off phenomena. Levodopa administered in a pulsatile manner may also lead to the induction of synaptic plasticity within the DA systems. In the ventral mesolimbic system, this could lead to the loss of behavioral flexibility, impulsive behavior, and cognitive impairment, whereas in the dorsal nigrostriatal system, this may underlie Levodopa-induced dyskinesia. Continuous administration of Levodopa may circumvent this sensitization process, enabling a therapeutic response without limbic and motor side effects.</AbstractText><CopyrightInformation>(c) 2008 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Grace</LastName><ForeName>Anthony A</ForeName><Initials>AA</Initials><AffiliationInfo><Affiliation>Department of Neuroscience, Center for Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. Graceaa@pitt.edu</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>DA15408</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>MH57440</GrantID><Acronym>MH</Acronym><Agency>NIMH 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="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson 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UI="D009714">Nucleus Accumbens</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011954">Receptors, Dopamine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013569">Synapses</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009435">Synaptic Transmission</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005680">gamma-Aminobutyric Acid</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>90</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>9</Month><Day>11</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>2</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>9</Month><Day>11</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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