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@ARTICLE{Byvaltcev:1010486,
      author       = {Byvaltcev, Egor and Behbood, Mahraz and Schleimer,
                      Jan-Hendrik and Gensch, Thomas and Semyanov, Alexey and
                      Schreiber, Susanne and Strauss, Ulf},
      title        = {{KCC}2 reverse mode helps to clear postsynaptically
                      released potassium at glutamatergic synapses},
      journal      = {Cell reports},
      volume       = {42},
      number       = {8},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {FZJ-2023-03081},
      pages        = {112934 -},
      year         = {2023},
      note         = {This project has received funding from the EuropeanResearch
                      Council (ERC) under the Union’s Horizon 2020 research an
                      innovation program (grant agreement no. 864243) and from the
                      Einstein FoundationBerlin (EP-2021-621).},
      abstract     = {Extracellular potassium [K+]o elevation during synaptic
                      activity retrogradely modifies presynaptic release and
                      astrocytic uptake of glutamate. Hence, local K+ clearance
                      and replenishment mechanisms are crucial regulators of
                      glutamatergic transmission and plasticity. Based on
                      recordings of astrocytic inward rectifier potassium current
                      IKir and K+-sensitive electrodes as sensors of [K+]o as well
                      as on in silico modeling, we demonstrate that the neuronal
                      K+-Cl- co-transporter KCC2 clears local perisynaptic [K+]o
                      during synaptic excitation by operating in an
                      activity-dependent reversed mode. In reverse mode, KCC2
                      replenishes K+ in dendritic spines and complements clearance
                      of [K+]o, therewith attenuating presynaptic glutamate
                      release and shortening LTP. We thus demonstrate a
                      physiological role of KCC2 in neuron-glial interactions and
                      regulation of synaptic signaling and plasticity through the
                      uptake of postsynaptically released K+.},
      cin          = {IBI-1},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IBI-1-20200312},
      pnm          = {5243 - Information Processing in Distributed Systems
                      (POF4-524)},
      pid          = {G:(DE-HGF)POF4-5243},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {37537840},
      UT           = {WOS:001051595700001},
      doi          = {10.1016/j.celrep.2023.112934},
      url          = {https://juser.fz-juelich.de/record/1010486},
}