Error-Related Functional Connectivity of the Habenula in Humans
Identifieur interne : 002B97 ( Main/Curation ); précédent : 002B96; suivant : 002B98Error-Related Functional Connectivity of the Habenula in Humans
Auteurs : Jaime S. Ide [États-Unis] ; Chiang-Shan R. Li [États-Unis]Source :
- Frontiers in Human Neuroscience [ 1662-5161 ] ; 2011.
Abstract
Error detection is critical to the shaping of goal-oriented behavior. Recent studies in non-human primates delineated a circuit involving the lateral habenula (LH) and ventral tegmental area (VTA) in error detection. Neurons in the LH increased activity, preceding decreased activity in the VTA, to a missing reward, indicating a feedforward signal from the LH to VTA. In the current study we used connectivity analyses to reveal this pathway in humans. In 59 adults performing a stop signal task during functional magnetic resonance imaging, we identified brain regions showing greater psychophysiological interaction with the habenula during stop error as compared to stop success trials. These regions included a cluster in the VTA/substantia nigra (SN), internal segment of globus pallidus, bilateral amygdala, and insula. Furthermore, using Granger causality and mediation analyses, we showed that the habenula Granger caused the VTA/SN, establishing the direction of this interaction, and that the habenula mediated the functional connectivity between the amygdala and VTA/SN during error processing. To our knowledge, these findings are the first to demonstrate a feedforward influence of the habenula on the VTA/SN during error detection in humans.
Url:
DOI: 10.3389/fnhum.2011.00025
PubMed: 21441989
PubMed Central: 3060701
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Error-Related Functional Connectivity of the Habenula in Humans</title><author><name sortKey="Ide, Jaime S" sort="Ide, Jaime S" uniqKey="Ide J" first="Jaime S." last="Ide">Jaime S. Ide</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Psychiatry, Yale University School of Medicine</institution><country>New Haven, CT, USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author><author><name sortKey="Li, Chiang Shan R" sort="Li, Chiang Shan R" uniqKey="Li C" first="Chiang-Shan R." last="Li">Chiang-Shan R. 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Ide</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Psychiatry, Yale University School of Medicine</institution><country>New Haven, CT, USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author><author><name sortKey="Li, Chiang Shan R" sort="Li, Chiang Shan R" uniqKey="Li C" first="Chiang-Shan R." last="Li">Chiang-Shan R. Li</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Department of Psychiatry, Yale University School of Medicine</institution><country>New Haven, CT, USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Department of Neurobiology, Yale University School of Medicine</institution><country>New Haven, CT, USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Interdepartmental Neuroscience Program, Yale University School of Medicine</institution><country>New Haven, CT, USA</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea></wicri:regionArea><wicri:regionArea># see nlm:aff region in country</wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Human Neuroscience</title><idno type="eISSN">1662-5161</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Error detection is critical to the shaping of goal-oriented behavior. Recent studies in non-human primates delineated a circuit involving the lateral habenula (LH) and ventral tegmental area (VTA) in error detection. Neurons in the LH increased activity, preceding decreased activity in the VTA, to a missing reward, indicating a feedforward signal from the LH to VTA. In the current study we used connectivity analyses to reveal this pathway in humans. In 59 adults performing a stop signal task during functional magnetic resonance imaging, we identified brain regions showing greater psychophysiological interaction with the habenula during stop error as compared to stop success trials. These regions included a cluster in the VTA/substantia nigra (SN), internal segment of globus pallidus, bilateral amygdala, and insula. Furthermore, using Granger causality and mediation analyses, we showed that the habenula Granger caused the VTA/SN, establishing the direction of this interaction, and that the habenula mediated the functional connectivity between the amygdala and VTA/SN during error processing. To our knowledge, these findings are the first to demonstrate a feedforward influence of the habenula on the VTA/SN during error detection in humans.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Abler, B" uniqKey="Abler B">B. Abler</name></author><author><name sortKey="Roebroeck, A" uniqKey="Roebroeck A">A. Roebroeck</name></author><author><name sortKey="Goebel, R" uniqKey="Goebel R">R. Goebel</name></author><author><name sortKey="Hose, A" uniqKey="Hose A">A. Hose</name></author><author><name sortKey="Schonfeldt Lecuona, C" uniqKey="Schonfeldt Lecuona C">C. Schonfeldt-Lecuona</name></author><author><name sortKey="Hole, G" uniqKey="Hole G">G. 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