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@ARTICLE{Halfmann:1021445,
      author       = {Halfmann, Claas and Rüland, Thomas and Müller, Frank and
                      Jehasse, Kevin and Kampa, Björn M.},
      title        = {{E}lectrophysiological properties of layer 2/3 pyramidal
                      neurons in the primary visual cortex of a retinitis
                      pigmentosa mouse model (rd10)},
      journal      = {Frontiers in cellular neuroscience},
      volume       = {17},
      issn         = {1662-5102},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {FZJ-2024-00741},
      pages        = {1258773},
      year         = {2023},
      note         = {This study was funded by the Deutsche
                      Forschungsgemeinschaft(DFG, German Research
                      Foundation)−368482240/GRK2416 andGRK2610: Innoretvision.},
      abstract     = {Retinal degeneration is one of the main causes of visual
                      impairment and blindness. One group of retinal degenerative
                      diseases, leading to the loss of photoreceptors, is
                      collectively termed retinitis pigmentosa. In this group of
                      diseases, the remaining retina is largely spared from
                      initial cell death making retinal ganglion cells an
                      interesting target for vision restoration methods. However,
                      it is unknown how downstream brain areas, in particular the
                      visual cortex, are affected by the progression of blindness.
                      Visual deprivation studies have shown dramatic changes in
                      the electrophysiological properties of visual cortex
                      neurons, but changes on a cellular level in retinitis
                      pigmentosa have not been investigated yet. Therefore, we
                      used the rd10 mouse model to perform patch-clamp recordings
                      of pyramidal neurons in layer 2/3 of the primary visual
                      cortex to screen for potential changes in
                      electrophysiological properties resulting from retinal
                      degeneration. Compared to wild-type C57BL/6 mice, we only
                      found an increase in intrinsic excitability around the time
                      point of maximal retinal degeneration. In addition, we saw
                      an increase in the current amplitude of spontaneous putative
                      inhibitory events after a longer progression of retinal
                      degeneration. However, we did not observe a long-lasting
                      shift in excitability after prolonged retinal degeneration.
                      Together, our results provide evidence of an intact visual
                      cortex with promising potential for future therapeutic
                      strategies to restore vision.},
      cin          = {IBI-1 / INM-10},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IBI-1-20200312 / I:(DE-Juel1)INM-10-20170113},
      pnm          = {5241 - Molecular Information Processing in Cellular Systems
                      (POF4-524) / GRK 2416 - GRK 2416: MultiSenses-MultiScales:
                      Neue Ansätze zur Aufklärung neuronaler multisensorischer
                      Integration (368482240) / GRK 2610 - GRK 2610: Innovative
                      Schnittstellen zur Retina für optimiertes künstliches
                      Sehen - InnoRetVision (424556709)},
      pid          = {G:(DE-HGF)POF4-5241 / G:(GEPRIS)368482240 /
                      G:(GEPRIS)424556709},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.3389/fncel.2023.1258773},
      url          = {https://juser.fz-juelich.de/record/1021445},
}