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@ARTICLE{Breithausen:141697,
      author       = {Breithausen, Björn and Kautzmann, Steffen and Boehlen,
                      Anne and Steinhäuser, Christian and Henneberger, Christian},
      title        = {{L}imited contribution of astroglial gap junction coupling
                      to buffering of extracellular {K}+ in {CA}1 stratum
                      radiatum.},
      journal      = {Glia},
      volume       = {68},
      number       = {5},
      issn         = {0894-1491},
      address      = {Bognor Regis [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {DZNE-2020-00028},
      pages        = {918-931},
      year         = {2019},
      abstract     = {Astrocytes form large networks, in which individual cells
                      are connected via gap junctions. It is thought that this
                      astroglial gap junction coupling contributes to the
                      buffering of extracellular K+ increases. However, it is
                      largely unknown how the control of extracellular K+ by
                      astroglial gap junction coupling depends on the underlying
                      activity patterns and on the magnitude of extracellular K+
                      increases. We explored this dependency in acute hippocampal
                      slices (CA1, stratum radiatum) by direct K+ -sensitive
                      microelectrode recordings and acute pharmacological
                      inhibition of gap junctions. K+ transients evoked by
                      synaptic and axonal activity were largely unaffected by
                      acute astroglial uncoupling in slices obtained from young
                      and adult rats. Iontophoretic K+ -application enabled us to
                      generate K+ gradients with defined spatial properties and
                      magnitude. By varying the K+ -iontophoresis position and
                      protocol, we found that acute pharmacological uncoupling
                      increases the amplitude of K+ transients once their initial
                      amplitude exceeded ~10 mM. Our experiments demonstrate
                      that the contribution of gap junction coupling to buffering
                      of extracellular K+ gradients is limited to large and
                      localized K+ increases.},
      keywords     = {Animals / Astrocytes: metabolism / CA1 Region, Hippocampal:
                      metabolism / Gap Junctions: metabolism / Membrane
                      Potentials: physiology / Neurons: metabolism / Potassium:
                      metabolism / Rats / Rats, Wistar / Synapses: metabolism},
      cin          = {U Preclinical Researchers - Bonn},
      ddc          = {610},
      cid          = {I:(DE-2719)7000005},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31743499},
      doi          = {10.1002/glia.23751},
      url          = {https://pub.dzne.de/record/141697},
}