dc.contributorMax Planck Inst Psychiat
dc.contributorHarvard Med Sch
dc.contributorMcLean Hosp
dc.contributorUniversidade Estadual Paulista (Unesp)
dc.contributorHeidelberg Univ
dc.contributorHelmholtz Zentrum Munchen
dc.contributorTech Univ Munich
dc.contributorGerman Ctr Neurodegenerat Dis DZNE
dc.contributorMax Planck Gesell
dc.date.accessioned2018-11-26T16:01:21Z
dc.date.available2018-11-26T16:01:21Z
dc.date.created2018-11-26T16:01:21Z
dc.date.issued2018-06-01
dc.identifierNature Neuroscience. New York: Nature Publishing Group, v. 21, n. 6, p. 803-+, 2018.
dc.identifier1097-6256
dc.identifierhttp://hdl.handle.net/11449/160318
dc.identifier10.1038/s41593-018-0151-z
dc.identifierWOS:000433232600008
dc.description.abstractThe interplay between corticotropin-releasing hormone (CRH) and the dopaminergic system has predominantly been studied in addiction and reward, while CRH-dopamine interactions in anxiety are scarcely understood. We describe a new population of CRH-expressing, GABAergic, long-range-projecting neurons in the extended amygdala that innervate the ventral tegmental area and alter anxiety following chronic CRH depletion. These neurons are part of a distinct CRH circuit that acts anxiolytically by positively modulating dopamine release.
dc.languageeng
dc.publisherNature Publishing Group
dc.relationNature Neuroscience
dc.relation15,207
dc.rightsAcesso restrito
dc.sourceWeb of Science
dc.titleChronic CRH depletion from GABAergic, long-range projection neurons in the extended amygdala reduces dopamine release and increases anxiety
dc.typeArtículos de revistas


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