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@ARTICLE{Kanellopoulos:890394,
      author       = {Kanellopoulos, Alexandros K. and Mariano, Vittoria and
                      Spinazzi, Marco and Woo, Young Jae and McLean, Colin and
                      Pech, Ulrike and Li, Ka Wan and Armstrong, J. Douglas and
                      Giangrande, Angela and Callaerts, Patrick and Smit, August
                      B. and Abrahams, Brett S. and Fiala, Andre and Achsel,
                      Tilmann and Bagni, Claudia},
      title        = {{A}ralar {S}equesters {GABA} into {H}yperactive
                      {M}itochondria, {C}ausing {S}ocial {B}ehavior {D}eficits},
      journal      = {Cell},
      volume       = {180},
      number       = {6},
      issn         = {0092-8674},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {FZJ-2021-00927},
      pages        = {1178 - 1197.e20},
      year         = {2020},
      abstract     = {Social 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.},
      cin          = {INM-9 / IAS-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-9-20140121 / I:(DE-Juel1)IAS-5-20120330},
      pnm          = {574 - Theory, modelling and simulation (POF3-574)},
      pid          = {G:(DE-HGF)POF3-574},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {32200800},
      UT           = {WOS:000520925300014},
      doi          = {10.1016/j.cell.2020.02.044},
      url          = {https://juser.fz-juelich.de/record/890394},
}