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@ARTICLE{Martineau:841726,
      author       = {Martineau, Magalie and Guzman, Raul and Fahlke, Christoph
                      and Klingauf, Jürgen},
      title        = {{VGLUT}1 functions as a glutamate/proton exchanger with
                      chloride channel activity in hippocampal glutamatergic
                      synapses},
      journal      = {Nature Communications},
      volume       = {8},
      number       = {1},
      issn         = {2041-1723},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {FZJ-2018-00034},
      pages        = {2279},
      year         = {2017},
      abstract     = {Glutamate is the major excitatory transmitter in the
                      vertebrate nervous system. To maintain synaptic efficacy,
                      recycling synaptic vesicles (SV) are refilled with glutamate
                      by vesicular glutamate transporters (VGLUTs). The dynamics
                      and mechanism of glutamate uptake in intact neurons are
                      still largely unknown. Here, we show by live-cell imaging
                      with pH- and chloride-sensitive fluorescent probes in
                      cultured hippocampal neurons of wild-type and
                      VGLUT1-deficient mice that in SVs VGLUT functions as a
                      glutamate/proton exchanger associated with a channel-like
                      chloride conductance. After endocytosis most internalized
                      Cl− is substituted by glutamate in an electrically, and
                      presumably osmotically, neutral manner, and this process is
                      driven by both the Cl− gradient itself and the proton
                      motive force provided by the vacuolar H+-ATPase. Our results
                      shed light on the transport mechanism of VGLUT under
                      physiological conditions and provide a framework for how
                      modulation of glutamate transport via Cl− and pH can
                      change synaptic strength.},
      cin          = {ICS-4},
      ddc          = {500},
      cid          = {I:(DE-Juel1)ICS-4-20110106},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29273736},
      UT           = {WOS:000418570600024},
      doi          = {10.1038/s41467-017-02367-6},
      url          = {https://juser.fz-juelich.de/record/841726},
}