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@ARTICLE{Kapell:241120,
      author       = {H. Kapell and L. Fazio and J. Dyckow and S. Schwarz and A.
                      Cruz-Herranz and C. Mayer and J. Campos and E. D Este and W.
                      Möbius and C. Cordano and A.-K. Pröbstel and M.
                      Gharagozloo and A. Zulji and V. Narayanan Naik and A.-K.
                      Delank and M. Cerina and T. Müntefering and C. Lerma-Martin
                      and J. K. Sonner and J. H. Sin and P. Disse and N. Rychlik
                      and K. Sabeur and M. Chavali and R. Srivastava and M.
                      Heidenreich and K. C. Fitzgerald and G. Seebohm and C.
                      Stadelmann and B. Hemmer and M. Platten$^*$ and T. J.
                      Jentsch and M. Engelhardt and T. Budde and K.-A. Nave and P.
                      A. Calabresi and M. A. Friese and A. J. Green and C. Acuna
                      and D. H. Rowitch and S. G. Meuth and L. Schirmer},
      title        = {{N}euron-oligodendrocyte potassium shuttling at nodes of
                      {R}anvier protects against inflammatory demyelination.},
      journal      = {The journal of clinical investigation},
      volume       = {133},
      number       = {7},
      issn         = {0021-9738},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DKFZ-2023-00240},
      pages        = {e164223},
      year         = {2023},
      note         = {2023 Apr 3;133(7):e164223},
      abstract     = {Multiple sclerosis (MS) is a progressive
                      inflammatory-demyelinating disease of the central nervous
                      system. Increasing evidence suggests that vulnerable neurons
                      in MS exhibit fatal metabolic exhaustion over time, a
                      phenomenon hypothesized to be caused by chronic
                      hyperexcitability. Axonal Kv7 (outward rectifying) and
                      oligodendroglial Kir4.1 (inward rectifying) potassium
                      channels have important roles in regulating neuronal
                      excitability at and around nodes of Ranvier. Here, we
                      studied the spatial and functional relationship between
                      neuronal Kv7 and oligodendroglial Kir4.1 channels and
                      assessed the transcriptional and functional signatures of
                      cortical and retinal projection neurons under physiological
                      and inflammatory-demyelinating conditions. We found that
                      both channels became dysregulated in MS and experimental
                      autoimmune encephalomyelitis (EAE) with Kir4.1 channels
                      being chronically downregulated and Kv7 channel subunits
                      being transiently upregulated during inflammatory
                      demyelination. Further, we observed that pharmacological Kv7
                      channel opening with retigabine reduced neuronal
                      hyperexcitability in human and EAE neurons, improved
                      clinical EAE signs and rescued neuronal pathology in
                      oligodendrocyte-Kir4.1-deficient mice. In summary, our
                      findings indicate that neuron-oligodendrocyte compensatory
                      interactions promote resilience through Kv7 and Kir4.1
                      channels and suggest pharmacological activation of nodal Kv7
                      channels as a neuroprotective strategy against inflammatory
                      demyelination.},
      keywords     = {Inflammation (Other) / Multiple sclerosis (Other) /
                      Neurodegeneration (Other) / Neuroscience (Other) / Potassium
                      channels (Other)},
      cin          = {D170 / HD01},
      ddc          = {610},
      cid          = {I:(DE-He78)D170-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36719741},
      doi          = {10.1172/JCI164223},
      url          = {https://inrepo02.dkfz.de/record/241120},
}