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@ARTICLE{Kherbouche:281346,
      author       = {Kherbouche, Oussama and Henning, Lukas and Niemann, Pia and
                      Geisen, Caroline and Seifert, Gerald and Henneberger,
                      Christian and Fleischmann, Bernd K and Steinhäuser,
                      Christian and Bedner, Peter},
      title        = {{I}nduced {O}verexpression of {C}onnexin43 in {A}strocytes
                      {A}ttenuates the {P}rogression of {E}xperimental {T}emporal
                      {L}obe {E}pilepsy.},
      journal      = {Neurochemical research},
      volume       = {50},
      number       = {5},
      issn         = {0364-3190},
      address      = {Dordrecht [u.a.]},
      publisher    = {Springer Science + Business Media B.V},
      reportid     = {DZNE-2025-01093},
      pages        = {303},
      year         = {2025},
      abstract     = {Astrocytic gap junctional communication plays a critical
                      role in regulating neuronal activity and network
                      synchronization, yet its precise contributions to brain
                      function and the pathogenesis of neurological disorders
                      remains incompletely understood. To address this, we
                      generated a transgenic mouse line with inducible,
                      astrocyte-specific overexpression of the gap junction
                      protein connexin43 (Cx43). In these mice, hippocampal
                      astrocytes exhibited markedly elevated Cx43 protein levels
                      and a ~ $20\%$ increase in intercellular gap junction
                      coupling. Enhanced coupling was accompanied by a reduction
                      in astrocytic cell volume and branching, without affecting
                      passive membrane properties or astrocyte density in the
                      hippocampus. Cx43 overexpression had no detectable impact on
                      adult neurogenesis in the dentate gyrus, nor did it alter
                      hippocampal synaptic efficacy or plasticity. Notably, in a
                      mouse model of temporal lobe epilepsy with hippocampal
                      sclerosis, astrocytic Cx43 overexpression attenuated chronic
                      epileptic activity and the extent of sclerosis, supporting
                      an antiepileptic role of the astroglial network.
                      Collectively, these findings enhance our understanding of
                      the functional relevance of astrocytic gap junction coupling
                      in health and disease, with potential implications for the
                      design of new treatment strategies.},
      keywords     = {Animals / Astrocytes: metabolism / Connexin 43:
                      biosynthesis / Connexin 43: genetics / Epilepsy, Temporal
                      Lobe: metabolism / Epilepsy, Temporal Lobe: pathology /
                      Mice, Transgenic / Mice / Disease Progression / Hippocampus:
                      metabolism / Hippocampus: pathology / Mice, Inbred C57BL /
                      Gap Junctions: metabolism / Male / Connexin 43 (Other) / EEG
                      (Other) / Electrophysiology (Other) / Gap junction coupling
                      (Other) / Hippocampal sclerosis (Other) / Temporal lobe
                      epilepsy (Other) / Connexin 43 (NLM Chemicals)},
      cin          = {AG Henneberger},
      ddc          = {610},
      cid          = {I:(DE-2719)1013029},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40965686},
      pmc          = {pmc:PMC12446404},
      doi          = {10.1007/s11064-025-04558-w},
      url          = {https://pub.dzne.de/record/281346},
}