000890394 001__ 890394
000890394 005__ 20230111074324.0
000890394 0247_ $$2doi$$a10.1016/j.cell.2020.02.044
000890394 0247_ $$2ISSN$$a0092-8674
000890394 0247_ $$2ISSN$$a1097-4172
000890394 0247_ $$2Handle$$a2128/27108
000890394 0247_ $$2altmetric$$aaltmetric:77874373
000890394 0247_ $$2pmid$$a32200800
000890394 0247_ $$2WOS$$aWOS:000520925300014
000890394 037__ $$aFZJ-2021-00927
000890394 082__ $$a610
000890394 1001_ $$0P:(DE-HGF)0$$aKanellopoulos, Alexandros K.$$b0
000890394 245__ $$aAralar Sequesters GABA into Hyperactive Mitochondria, Causing Social Behavior Deficits
000890394 260__ $$aNew York, NY$$bElsevier$$c2020
000890394 3367_ $$2DRIVER$$aarticle
000890394 3367_ $$2DataCite$$aOutput Types/Journal article
000890394 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1612364842_8932
000890394 3367_ $$2BibTeX$$aARTICLE
000890394 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000890394 3367_ $$00$$2EndNote$$aJournal Article
000890394 520__ $$aSocial impairment is frequently associated with mitochondrial dysfunction and altered neurotransmission. Although mitochondrial function is crucial for brain homeostasis, it remains unknown whether mitochondrial disruption contributes to social behavioral deficits. Here, we show that Drosophila mutants in the homolog of the human CYFIP1, a gene linked to autism and schizophrenia, exhibit mitochondrial hyperactivity and altered group behavior. We identify the regulation of GABA availability by mitochondrial activity as a biologically relevant mechanism and demonstrate its contribution to social behavior. Specifically, increased mitochondrial activity causes gamma aminobutyric acid (GABA) sequestration in the mitochondria, reducing GABAergic signaling and resulting in social deficits. Pharmacological and genetic manipulation of mitochondrial activity or GABA signaling corrects the observed abnormalities. We identify Aralar as the mitochondrial transporter that sequesters GABA upon increased mitochondrial activity. This study increases our understanding of how mitochondria modulate neuronal homeostasis and social behavior under physiopathological conditions.
000890394 536__ $$0G:(DE-HGF)POF3-574$$a574 - Theory, modelling and simulation (POF3-574)$$cPOF3-574$$fPOF III$$x0
000890394 588__ $$aDataset connected to CrossRef
000890394 7001_ $$0P:(DE-HGF)0$$aMariano, Vittoria$$b1
000890394 7001_ $$0P:(DE-HGF)0$$aSpinazzi, Marco$$b2
000890394 7001_ $$0P:(DE-HGF)0$$aWoo, Young Jae$$b3
000890394 7001_ $$0P:(DE-HGF)0$$aMcLean, Colin$$b4
000890394 7001_ $$0P:(DE-HGF)0$$aPech, Ulrike$$b5
000890394 7001_ $$0P:(DE-Juel1)171511$$aLi, Ka Wan$$b6
000890394 7001_ $$0P:(DE-HGF)0$$aArmstrong, J. Douglas$$b7
000890394 7001_ $$0P:(DE-HGF)0$$aGiangrande, Angela$$b8
000890394 7001_ $$0P:(DE-HGF)0$$aCallaerts, Patrick$$b9
000890394 7001_ $$0P:(DE-HGF)0$$aSmit, August B.$$b10
000890394 7001_ $$0P:(DE-HGF)0$$aAbrahams, Brett S.$$b11
000890394 7001_ $$0P:(DE-HGF)0$$aFiala, Andre$$b12
000890394 7001_ $$0P:(DE-HGF)0$$aAchsel, Tilmann$$b13
000890394 7001_ $$0P:(DE-HGF)0$$aBagni, Claudia$$b14$$eCorresponding author
000890394 773__ $$0PERI:(DE-600)2001951-8$$a10.1016/j.cell.2020.02.044$$gVol. 180, no. 6, p. 1178 - 1197.e20$$n6$$p1178 - 1197.e20$$tCell$$v180$$x0092-8674$$y2020
000890394 8564_ $$uhttps://juser.fz-juelich.de/record/890394/files/Author%20version.pdf$$yPublished on 2020-03-19. Available in OpenAccess from 2021-03-19.
000890394 909CO $$ooai:juser.fz-juelich.de:890394$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000890394 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-HGF)0$$aForschungszentrum Jülich$$b7$$kFZJ
000890394 9130_ $$0G:(DE-HGF)POF3-574$$1G:(DE-HGF)POF3-570$$2G:(DE-HGF)POF3-500$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bKey Technologies$$lDecoding the Human Brain$$vTheory, modelling and simulation$$x0
000890394 9131_ $$0G:(DE-HGF)POF4-525$$1G:(DE-HGF)POF4-520$$2G:(DE-HGF)POF4-500$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$9G:(DE-HGF)POF4-5252$$aDE-HGF$$bKey Technologies$$lNatural, Artificial and Cognitive Information Processing$$vDecoding Brain Organization and Dysfunction$$x0
000890394 9141_ $$y2021
000890394 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2020-09-03
000890394 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2020-09-03
000890394 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews$$d2020-09-03
000890394 915__ $$0StatID:(DE-HGF)1190$$2StatID$$aDBCoverage$$bBiological Abstracts$$d2020-09-03
000890394 915__ $$0StatID:(DE-HGF)0600$$2StatID$$aDBCoverage$$bEbsco Academic Search$$d2020-09-03
000890394 915__ $$0LIC:(DE-HGF)CCBYNCND4$$2HGFVOC$$aCreative Commons Attribution-NonCommercial-NoDerivs CC BY-NC-ND 4.0
000890394 915__ $$0StatID:(DE-HGF)0530$$2StatID$$aEmbargoed OpenAccess
000890394 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences$$d2020-09-03
000890394 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2020-09-03
000890394 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2020-09-03
000890394 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bASC$$d2020-09-03
000890394 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2020-09-03
000890394 915__ $$0StatID:(DE-HGF)0420$$2StatID$$aNationallizenz$$d2020-09-03$$wger
000890394 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2020-09-03
000890394 920__ $$lyes
000890394 9201_ $$0I:(DE-Juel1)INM-9-20140121$$kINM-9$$lComputational Biomedicine$$x0
000890394 9201_ $$0I:(DE-Juel1)IAS-5-20120330$$kIAS-5$$lComputational Biomedicine$$x1
000890394 980__ $$ajournal
000890394 980__ $$aVDB
000890394 980__ $$aUNRESTRICTED
000890394 980__ $$aI:(DE-Juel1)INM-9-20140121
000890394 980__ $$aI:(DE-Juel1)IAS-5-20120330
000890394 9801_ $$aFullTexts