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@ARTICLE{Timmermann:257561,
      author       = {Timmermann, Aline and Tascio, Dario and Jabs, Ronald and
                      Boehlen, Anne and Domingos, Catia and Skubal, Magdalena and
                      Huang, Wenhui and Kirchhoff, Frank and Henneberger,
                      Christian and Bilkei-Gorzo, Andras and Seifert, Gerald and
                      Steinhäuser, Christian},
      title        = {{D}ysfunction of {NG}2 glial cells affects neuronal
                      plasticity and behavior.},
      journal      = {Glia},
      volume       = {71},
      number       = {6},
      issn         = {0894-1491},
      address      = {Bognor Regis [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {DZNE-2023-00441},
      pages        = {1481 - 1501},
      year         = {2023},
      abstract     = {NG2 glia represents a distinct type of macroglial cells in
                      the CNS and is unique among glia because they receive
                      synaptic input from neurons. They are abundantly present in
                      white and gray matter. While the majority of white matter
                      NG2 glia differentiates into oligodendrocytes, the
                      physiological impact of gray matter NG2 glia and their
                      synaptic input are still ill defined. Here, we asked whether
                      dysfunctional NG2 glia affect neuronal signaling and
                      behavior. We generated mice with inducible deletion of the
                      K+ channel Kir4.1 in NG2 glia and performed comparative
                      electrophysiological, immunohistochemical, molecular and
                      behavioral analyses. Kir4.1 was deleted at postnatal day
                      23-26 (recombination efficiency about $75\%)$ and mice were
                      investigated 3-8 weeks later. Notably, these mice with
                      dysfunctional NG2 glia demonstrated improved spatial memory
                      as revealed by testing new object location recognition while
                      working and social memory remained unaffected. Focussing on
                      the hippocampus, we found that loss of Kir4.1 potentiated
                      synaptic depolarizations of NG2 glia and stimulated the
                      expression of myelin basic protein while proliferation and
                      differentiation of hippocampal NG2 glia remained largely
                      unaffected. Mice with targeted deletion of the K+ channel in
                      NG2 glia showed impaired long-term potentiation at CA3-CA1
                      synapses, which could be fully rescued by extracellular
                      application of a TrkB receptor agonist. Our data demonstrate
                      that proper NG2 glia function is important for normal brain
                      function and behavior.},
      keywords     = {Mice / Animals / Proteoglycans: metabolism / Neuroglia:
                      metabolism / Neurons: metabolism / Oligodendroglia:
                      metabolism / Neuronal Plasticity / Antigens: metabolism /
                      Kir4.1 (Other) / NG2 glia (Other) / myelination (Other) /
                      neuron-glia signaling (Other) / neuronal plasticity (Other)
                      / Proteoglycans (NLM Chemicals) / Antigens (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:36802096},
      doi          = {10.1002/glia.24352},
      url          = {https://pub.dzne.de/record/257561},
}