Goal-directed and habitual control in the basal ganglia: implications for Parkinson’s disease
Identifieur interne : 000586 ( Pmc/Curation ); précédent : 000585; suivant : 000587Goal-directed and habitual control in the basal ganglia: implications for Parkinson’s disease
Auteurs : Peter Redgrave [Royaume-Uni] ; Manuel Rodriguez [Espagne] ; Yoland Smith [États-Unis] ; Maria C. Rodriguez-Oroz [Espagne] ; Stephane Lehericy [France] ; Hagai Bergman [Israël] ; Yves Agid [France] ; Mahlon R. Delong [États-Unis] ; Jose A. Obeso [Espagne]Source :
- Nature reviews. Neuroscience [ 1471-003X ] ; 2010.
Abstract
Progressive loss of the ascending dopaminergic projection in the basal ganglia is a fundamental pathological feature of Parkinson’s disease. Studies in animals and humans have identified spatially segregated functional territories in the basal ganglia for the control of goal-directed and habitual actions. In patients with Parkinson’s disease the loss of dopamine is predominantly in the posterior putamen, a region of the basal ganglia associated with the control of habitual behaviour. These patients may therefore be forced into a progressive reliance on the goal-directed mode of action control that is mediated by comparatively preserved processing in the rostromedial striatum. Thus, many of their behavioural difficulties may reflect a loss of normal automatic control owing to distorting output signals from habitual control circuits, which impede the expression of goal-directed action.
Url:
DOI: 10.1038/nrn2915
PubMed: 20944662
PubMed Central: 3124757
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<front><div type="abstract" xml:lang="en"><p id="P1">Progressive loss of the ascending dopaminergic projection in the basal ganglia is a fundamental pathological feature of Parkinson’s disease. Studies in animals and humans have identified spatially segregated functional territories in the basal ganglia for the control of goal-directed and habitual actions. In patients with Parkinson’s disease the loss of dopamine is predominantly in the posterior putamen, a region of the basal ganglia associated with the control of habitual behaviour. These patients may therefore be forced into a progressive reliance on the goal-directed mode of action control that is mediated by comparatively preserved processing in the rostromedial striatum. Thus, many of their behavioural difficulties may reflect a loss of normal automatic control owing to distorting output signals from habitual control circuits, which impede the expression of goal-directed action.</p>
</div>
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<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
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<title-group><article-title>Goal-directed and habitual control in the basal ganglia: implications for Parkinson’s disease</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Redgrave</surname>
<given-names>Peter</given-names>
</name>
<xref ref-type="aff" rid="A1">*</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Rodriguez</surname>
<given-names>Manuel</given-names>
</name>
<xref ref-type="aff" rid="A2">‡</xref>
<xref ref-type="aff" rid="A3">§</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Smith</surname>
<given-names>Yoland</given-names>
</name>
<xref ref-type="aff" rid="A4">||</xref>
<xref ref-type="aff" rid="A5">¶</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Rodriguez-Oroz</surname>
<given-names>Maria C.</given-names>
</name>
<xref ref-type="aff" rid="A3">§</xref>
<xref ref-type="aff" rid="A6">#</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lehericy</surname>
<given-names>Stephane</given-names>
</name>
<xref ref-type="aff" rid="A7">**</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bergman</surname>
<given-names>Hagai</given-names>
</name>
<xref ref-type="aff" rid="A8">‡‡</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Agid</surname>
<given-names>Yves</given-names>
</name>
<xref ref-type="aff" rid="A9">§§</xref>
</contrib>
<contrib contrib-type="author"><name><surname>DeLong</surname>
<given-names>Mahlon R.</given-names>
</name>
<xref ref-type="aff" rid="A5">¶</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Obeso</surname>
<given-names>Jose A.</given-names>
</name>
<xref ref-type="aff" rid="A3">§</xref>
<xref ref-type="aff" rid="A6">#</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>*</label>
Neuroscience Research Unit, Department of Psychology, University of Sheffield, S10 2TP, UK.</aff>
<aff id="A2"><label>‡</label>
Department of Physiology, Medical School, University of La Laguna, Tenerife, 38201, Spain.</aff>
<aff id="A3"><label>§</label>
Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto Carlos III, Ministerio de Investigacion y Ciencias, 28038, Spain.</aff>
<aff id="A4"><label>||</label>
Yerkes National Primate Research Center, Emory University, Atlanta, Georgia 30329, USA.</aff>
<aff id="A5"><label>¶</label>
Department of Neurology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.</aff>
<aff id="A6"><label>#</label>
Movement Disorders Group, Neurosciences Division, CIMA and Department of Neurology and Neurosurgery, Clínica Universidad de Navarra, Pamplona, 31008, Spain.</aff>
<aff id="A7"><label>**</label>
Centre de NeuroImagerie de Recherche (CENIR), Institut du Cerveau et de la Moelle épinière (ICM), Universite Pierre et Marie Curie, Inserm U975, CNRS 7225, Groupe Hospitalier Pitié-Salpêtrière, 75013, Paris, France.</aff>
<aff id="A8"><label>‡‡</label>
Hebrew University, Hadassah Medical School, Jerusalem 91120, Israel.</aff>
<aff id="A9"><label>§§</label>
Institut du Cerveau et de la Moelle épinière (ICM), 75013, Paris, France.</aff>
<author-notes><corresp id="CR1">Correspondence to P.R. and J.O. <email>P.Redgrave@sheffield.ac.uk</email>
; <email>jobeso@unav.es</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>9</day>
<month>6</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="epub"><day>14</day>
<month>10</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="ppub"><month>11</month>
<year>2010</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>28</day>
<month>6</month>
<year>2011</year>
</pub-date>
<volume>11</volume>
<issue>11</issue>
<fpage>760</fpage>
<lpage>772</lpage>
<permissions><copyright-statement>© 2010 Macmillan Publishers Limited. All rights reserved</copyright-statement>
<copyright-year>2010</copyright-year>
</permissions>
<abstract><p id="P1">Progressive loss of the ascending dopaminergic projection in the basal ganglia is a fundamental pathological feature of Parkinson’s disease. Studies in animals and humans have identified spatially segregated functional territories in the basal ganglia for the control of goal-directed and habitual actions. In patients with Parkinson’s disease the loss of dopamine is predominantly in the posterior putamen, a region of the basal ganglia associated with the control of habitual behaviour. These patients may therefore be forced into a progressive reliance on the goal-directed mode of action control that is mediated by comparatively preserved processing in the rostromedial striatum. Thus, many of their behavioural difficulties may reflect a loss of normal automatic control owing to distorting output signals from habitual control circuits, which impede the expression of goal-directed action.</p>
</abstract>
<funding-group><award-group><funding-source country="United Kingdom">Wellcome Trust : </funding-source>
<award-id>091409 || WT</award-id>
</award-group>
</funding-group>
</article-meta>
</front>
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