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dc.contributor.authorPetrelli, Francesco
dc.contributor.authorDallérac, Glenn
dc.contributor.authorPucci, Luca
dc.contributor.authorCali, Corrado
dc.contributor.authorZehnder, Tamara
dc.contributor.authorSultan, Sébastien
dc.contributor.authorLecca, Salvatore
dc.contributor.authorChicca, Andrea
dc.contributor.authorIvanov, Andrei
dc.contributor.authorAsensio, Cédric S.
dc.contributor.authorGundersen, Vidar
dc.contributor.authorToni, Nicolas
dc.contributor.authorKnott, Graham William
dc.contributor.authorMagara, Fulvio
dc.contributor.authorGertsch, Jürg
dc.contributor.authorKirchhoff, Frank
dc.contributor.authorDéglon, Nicole
dc.contributor.authorGiros, Bruno
dc.contributor.authorEdwards, Robert H.
dc.contributor.authorMothet, Jean-Pierre
dc.contributor.authorBezzi, Paola
dc.date.accessioned2018-09-03T13:25:50Z
dc.date.available2018-09-03T13:25:50Z
dc.date.issued2018-08-20
dc.identifier.citationPetrelli F, Dallérac G, Pucci L, Calì C, Zehnder T, et al. (2018) Dysfunction of homeostatic control of dopamine by astrocytes in the developing prefrontal cortex leads to cognitive impairments. Molecular Psychiatry. Available: http://dx.doi.org/10.1038/s41380-018-0226-y.
dc.identifier.issn1359-4184
dc.identifier.issn1476-5578
dc.identifier.doi10.1038/s41380-018-0226-y
dc.identifier.urihttp://hdl.handle.net/10754/628466
dc.description.abstractAstrocytes orchestrate neural development by powerfully coordinating synapse formation and function and, as such, may be critically involved in the pathogenesis of neurodevelopmental abnormalities and cognitive deficits commonly observed in psychiatric disorders. Here, we report the identification of a subset of cortical astrocytes that are competent for regulating dopamine (DA) homeostasis during postnatal development of the prefrontal cortex (PFC), allowing for optimal DA-mediated maturation of excitatory circuits. Such control of DA homeostasis occurs through the coordinated activity of astroglial vesicular monoamine transporter 2 (VMAT2) together with organic cation transporter 3 and monoamine oxidase type B, two key proteins for DA uptake and metabolism. Conditional deletion of VMAT2 in astrocytes postnatally produces loss of PFC DA homeostasis, leading to defective synaptic transmission and plasticity as well as impaired executive functions. Our findings show a novel role for PFC astrocytes in the DA modulation of cognitive performances with relevance to psychiatric disorders.
dc.description.sponsorshipWe would like to thank G. Carmignoto and C. Lüscher for their discussions and comments on the manuscript; K. Tan and M. Mameli for the in vivo electrophysiology of aVMAT2cKO mice; M. Rey and V. Zimmer for producing the lentivirus and performing the stereotactic surgery; C. Bellone and S. Bariselli for providing virus and advices for optogenetic experiments; the Division of Pharmacology and Toxicology and E. Grouzmann for quantifying brain monoamines; P. Fossier for sharing his electrophysiological equipment; J. Marchaland for her technical support; and J. Gremion for his help with the immunohistochemistry experiments. The study was supported by grants from the Swiss National Foundation NCCR 'Synapsy' (51NF40-158776) and 'Transcure' (51NF40-160620) to PB, operating grants from the Agence National de la Recherche (ANR-09-MNPS-022-01), Fondation pour la Recherche Médicale (Equipe FRM DEQ20150331734), CNRS, Université Aix-Marseille and Conseil Régional Provence Alpes Côte d'Azur to JPM, and NSERC RGPIN grant 385732-2012 to B.G.
dc.publisherSpringer Nature
dc.relation.urlhttps://www.nature.com/articles/s41380-018-0226-y
dc.rightsThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.titleDysfunction of homeostatic control of dopamine by astrocytes in the developing prefrontal cortex leads to cognitive impairments
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.identifier.journalMolecular Psychiatry
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionDepartment of Fundamental Neurosciences, University of Lausanne, CH-1005, Lausanne, Switzerland
dc.contributor.institutionCentre de Recherche en Neurobiologie et Neurophysiologie de Marseille, Aix-Marseille Université UMR7286 CNRS, 13344, Marseille, Cedex 15, France
dc.contributor.institutionInstitute of Biochemistry and Molecular Medicine (IBMM), University of Bern, Buehlstrasse, 28 3012, Bern, Switzerland
dc.contributor.institution“Biophotonics and Synapse Physiopathology” Team, UMR9188 CNRS – ENS Paris Saclay, 91405, Orsay, France
dc.contributor.institutionDepartments of Neurology and Physiology, University of California San Francisco, San Francisco, CA, 94158, USA
dc.contributor.institutionCMBN, Rikshospitalet, University of Oslo, Oslo, Norway
dc.contributor.institutionBioEM Facility, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, CH-1015, Lausanne, Switzerland
dc.contributor.institutionCentre for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital Center, University of Lausanne, CH-1015, Lausanne, Switzerland
dc.contributor.institutionDepartment of Molecular Physiology, University of Saarland, D-66421, Homburg, Germany
dc.contributor.institutionNeuroscience Research Center, Lausanne University Hospital, CH-1011, Lausanne, Switzerland
dc.contributor.institutionDepartment of Clinical Neurosciences, Lausanne University Hospital, Lausanne, Switzerland
dc.contributor.institutionINSERM, UMRS 1130; CNRS, UMR 8246; Sorbonne University UPMC, Neuroscience Paris-Seine, F-75005, Paris, France
dc.contributor.institutionDepartment of Psychiatry, Douglas Mental Health University Institute, McGill University, Montreal, Quebec, H4H1R3, Canada
kaust.personCali, Corrado
refterms.dateFOA2018-09-04T13:23:37Z
dc.date.published-online2018-08-20
dc.date.published-print2020-04


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This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Except where otherwise noted, this item's license is described as This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.