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@ARTICLE{Mitlasczki:283024,
      author       = {Mitlasóczki, Bence and Gutiérrez Gómez, Adrián and
                      Kamali, Midia and Babushkina, Natalia and Baues, Mayan and
                      Kück, Laura and Haubrich, André Nathan and Tamiolakis,
                      Theodoros and Breuer, Annika and Granak, Simon and
                      Schwering-Sohnrey, Merlin and Gerhauser, Ingo and
                      Baumgärtner, Wolfgang and Schwarz, Martin Karl and Ewell,
                      Laura and Opitz, Thoralf and Pitsch, Julika and Musall,
                      Simon and Surges, Rainer and Mormann, Florian and Beck,
                      Heinz and Wenzel, Michael},
      title        = {{H}ippocampal spreading depolarization as a driver of
                      postictal ambulation.},
      journal      = {Science translational medicine},
      volume       = {17},
      number       = {816},
      issn         = {1946-6234},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DZNE-2025-01436},
      pages        = {eadv3260},
      year         = {2025},
      abstract     = {Postseizure (postictal) symptoms are regularly encountered
                      in epilepsy and can be life threatening, yet their
                      neurobiological underpinnings remain understudied. Using
                      two-photon or widefield imaging, field potential and unit
                      recordings, optogenetics, and basic behavioral assessment
                      under healthy conditions or viral encephalitis, we studied
                      seizures and postictal symptoms in mice. We show a
                      propensity of the hippocampus for seizure-associated
                      spreading depolarization (sSD). Through optogenetic
                      stimulation, we provide evidence that induced isolated
                      hippocampal SD is sufficient to elicit postictal ambulation
                      (PIA), whereas induced isolated seizure-like episodes are
                      not. Furthermore, PIA occurred in the absence of SD
                      progression to the neocortex. In addition, we analyzed
                      Behnke-Fried depth-electrode recordings in four patients
                      with focal epilepsy. Of 13 recorded seizures, we observed
                      five slow shifts at seizure termination in the regionwise
                      analysis that could reflect putative sSD. In support of our
                      experiments in mice, we also found an increased
                      vulnerability of the human temporomesial system (hippocampus
                      and amygdala) for this phenomenon and longer recovery times
                      of affected as compared with nonaffected brain regions. This
                      work suggests sSD as a previously underrecognized
                      pathoclinical entity underlying distinct postictal symptoms
                      in epilepsy.},
      keywords     = {Animals / Hippocampus: physiopathology / Humans / Seizures:
                      physiopathology / Male / Female / Walking: physiology / Mice
                      / Mice, Inbred C57BL / Optogenetics / Electroencephalography
                      / Adult},
      cin          = {Bonn common},
      ddc          = {500},
      cid          = {I:(DE-2719)6000011},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40961224},
      doi          = {10.1126/scitranslmed.adv3260},
      url          = {https://pub.dzne.de/record/283024},
}