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@ARTICLE{Graf:157766,
      author       = {Graf, Jürgen and Zhang, Chuanqiang and Marguet, Stephan
                      and Herrmann, Tanja and Flossmann, Tom and Hinsch, Robin and
                      Rahmati, Vahid and Guenther, Madlen and Frahm, Christiane
                      and Urbach, Anja and Neves, Ricardo Melo and Witte, Otto W
                      and Kiebel, Stefan J and Isbrandt, Dirk and Hübner,
                      Christian A and Holthoff, Knut and Kirmse, Knut},
      title        = {{A} limited role of {NKCC}1 in telencephalic glutamatergic
                      neurons for developing hippocampal network dynamics and
                      behavior.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {118},
      number       = {14},
      issn         = {1091-6490},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DZNE-2021-01223},
      pages        = {e2014784118},
      year         = {2021},
      abstract     = {NKCC1 is the primary transporter mediating chloride uptake
                      in immature principal neurons, but its role in the
                      development of in vivo network dynamics and cognitive
                      abilities remains unknown. Here, we address the function of
                      NKCC1 in developing mice using electrophysiological,
                      optical, and behavioral approaches. We report that NKCC1
                      deletion from telencephalic glutamatergic neurons decreases
                      in vitro excitatory actions of γ-aminobutyric acid (GABA)
                      and impairs neuronal synchrony in neonatal hippocampal brain
                      slices. In vivo, it has a minor impact on correlated
                      spontaneous activity in the hippocampus and does not affect
                      network activity in the intact visual cortex. Moreover,
                      long-term effects of the developmental NKCC1 deletion on
                      synaptic maturation, network dynamics, and behavioral
                      performance are subtle. Our data reveal a neural network
                      function of NKCC1 in hippocampal glutamatergic neurons in
                      vivo, but challenge the hypothesis that NKCC1 is essential
                      for major aspects of hippocampal development.},
      keywords     = {Animals / Animals, Newborn / Glutamic Acid: metabolism /
                      Hippocampus: growth $\&$ development / Mice / Nerve Net /
                      Neurons: metabolism / Solute Carrier Family 12, Member 2:
                      physiology / Synapses: metabolism / Visual Cortex:
                      physiology / gamma-Aminobutyric Acid: metabolism / GABA
                      (Other) / NKCC1 (Other) / development (Other) / hippocampus
                      (Other) / in vivo (Other)},
      cin          = {AG Isbrandt},
      ddc          = {500},
      cid          = {I:(DE-2719)1011003},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33782119},
      pmc          = {pmc:PMC8040628},
      doi          = {10.1073/pnas.2014784118},
      url          = {https://pub.dzne.de/record/157766},
}