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@ARTICLE{Petzold:163279,
      author       = {Petzold, Gabor C and Dreier, Jens P.},
      title        = {{S}preading depolarization evoked by endothelin-1 is
                      inhibited by octanol but not by carbenoxolone},
      journal      = {Brain hemorrhages},
      volume       = {2},
      number       = {1},
      issn         = {2589-238X},
      address      = {[Amsterdam]},
      publisher    = {Elsevier B.V.},
      reportid     = {DZNE-2022-00059},
      pages        = {6 - 14},
      year         = {2021},
      note         = {CC BY-NC-ND},
      abstract     = {Spreading depolarization (SD) has been implicated in the
                      pathogenesis of delayed cerebral ischemia (DCI) after
                      subarachnoid hemorrhage. Endothelin-1 (ET-1) is a powerful
                      trigger of SD and may be involved in DCI. The SD-causing
                      mechanism is assumed to result from ET-1-induced
                      microarterial spasm and ischemia. However, ET-1 is also a
                      potent, astrocyte-specific gap junction (GJ) inhibitor.
                      There are two competing hypotheses on the role of astrocytic
                      GJs in SD. One postulates that they mediate SDs, since
                      long-chain alcohols such as octanol inhibit GJs and inhibit
                      SD at high concentrations. The other postulates that
                      astrocytic GJs protect against SD and that their inhibition
                      increases susceptibility to SD and SD velocity. Here, we
                      found in rats that brain topical application of
                      carbenoxolone, a more specific GJ inhibitor, failed to
                      inhibit ET-1-induced SDs in vivo, whereas octanol, a less
                      specific GJ inhibitor, partially blocked them at high
                      concentrations. These results suggest that GJs are not
                      required for initiation or propagation of ET-1-induced SDs,
                      and that octanol inhibits SDs by effects unrelated to GJs.
                      The results do not exclude that the specific inhibition of
                      astrocytic GJs by ET-1 contributes to the generation of SDs,
                      which should be further investigated in future studies.},
      cin          = {AG Petzold},
      ddc          = {610},
      cid          = {I:(DE-2719)1013020},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1016/j.hest.2020.08.002},
      url          = {https://pub.dzne.de/record/163279},
}