Physiology of the Normal and Dopamine-Depleted Basal Ganglia : Insights into Levodopa Pharmacotherapy
Identifieur interne : 001138 ( PascalFrancis/Checkpoint ); précédent : 001137; suivant : 001139Physiology of the Normal and Dopamine-Depleted Basal Ganglia : Insights into Levodopa Pharmacotherapy
Auteurs : Anthony A. Grace [États-Unis]Source :
- Movement disorders [ 0885-3185 ] ; 2008.
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- Pascal (Inist)
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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.
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">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"><inist:fA14 i1="01"><s1>Department of Neuroscience, Center for Neuroscience, University of Pittsburgh</s1><s2>Pittsburgh, Pennsylvania</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Psychiatry, Center for Neuroscience, University of Pittsburgh</s1><s2>Pittsburgh, Pennsylvania</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation><affiliation wicri:level="4"><inist:fA14 i1="03"><s1>Departments of Psychology, Center for Neuroscience, University of Pittsburgh</s1><s2>Pittsburgh, Pennsylvania</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><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">INIST</idno><idno type="inist">08-0466146</idno><date when="2008">2008</date><idno type="stanalyst">PASCAL 08-0466146 INIST</idno><idno type="RBID">Pascal:08-0466146</idno><idno type="wicri:Area/PascalFrancis/Corpus">001135</idno><idno type="wicri:Area/PascalFrancis/Curation">001B84</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">001138</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">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"><inist:fA14 i1="01"><s1>Department of Neuroscience, Center for Neuroscience, University of Pittsburgh</s1><s2>Pittsburgh, Pennsylvania</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Psychiatry, Center for Neuroscience, University of Pittsburgh</s1><s2>Pittsburgh, Pennsylvania</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation><affiliation wicri:level="4"><inist:fA14 i1="03"><s1>Departments of Psychology, Center for Neuroscience, University of Pittsburgh</s1><s2>Pittsburgh, Pennsylvania</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><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" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basal ganglion</term><term>Dopamine</term><term>Levodopa</term><term>Nervous system diseases</term><term>Nucleus accumbens</term><term>Parkinson disease</term><term>Physiology</term><term>Potentiation</term><term>Synaptic plasticity</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Physiologie</term><term>Dopamine</term><term>Noyau gris central</term><term>Lévodopa</term><term>Noyau accumbens</term><term>Potentialisation</term><term>Plasticité synaptique</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><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>23</s2></fA05><fA06><s3>SUP3</s3></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Physiology of the Normal and Dopamine-Depleted Basal Ganglia : Insights into Levodopa Pharmacotherapy</s1></fA08><fA09 i1="01" i2="1" l="ENG"><s1>Levodopa Treatment and Motor Complications in Parkinson's Disease: Scientific Basis and Therapeutic Approaches</s1></fA09><fA11 i1="01" i2="1"><s1>GRACE (Anthony A.)</s1></fA11><fA12 i1="01" i2="1"><s1>OLANOW (C. Warren)</s1><s9>ed.</s9></fA12><fA12 i1="02" i2="1"><s1>LEES (Andrew)</s1><s9>limin.</s9></fA12><fA12 i1="03" i2="1"><s1>OBESO (Jose)</s1><s9>limin.</s9></fA12><fA14 i1="01"><s1>Department of Neuroscience, Center for Neuroscience, University of Pittsburgh</s1><s2>Pittsburgh, Pennsylvania</s2><s3>USA</s3><sZ>1 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Psychiatry, Center for Neuroscience, University of Pittsburgh</s1><s2>Pittsburgh, Pennsylvania</s2><s3>USA</s3><sZ>1 aut.</sZ></fA14><fA14 i1="03"><s1>Departments of Psychology, Center for Neuroscience, University of Pittsburgh</s1><s2>Pittsburgh, Pennsylvania</s2><s3>USA</s3><sZ>1 aut.</sZ></fA14><fA15 i1="01"><s1>Department of Neurology, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>1 aut.</sZ></fA15><fA15 i1="02"><s1>Department of Neurology, Reta Lila Institute of Neurological Studies</s1><s2>London</s2><s3>GBR</s3><sZ>2 aut.</sZ></fA15><fA15 i1="03"><s1>Department of Neurology, University of Navarra</s1><s2>Pamplona</s2><s3>ESP</s3><sZ>3 aut.</sZ></fA15><fA20><s2>S560-S569</s2></fA20><fA21><s1>2008</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000185584120070</s5></fA43><fA44><s0>0000</s0><s1>© 2008 INIST-CNRS. 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Grace</name></region><name sortKey="Grace, Anthony A" sort="Grace, Anthony A" uniqKey="Grace A" first="Anthony A." last="Grace">Anthony A. Grace</name><name sortKey="Grace, Anthony A" sort="Grace, Anthony A" uniqKey="Grace A" first="Anthony A." last="Grace">Anthony A. Grace</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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