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@ARTICLE{Landmann:843663,
      author       = {Landmann, Julia and Richter, Franziska and Oros-Peusquens,
                      Ana-Maria and Shah, N. J. and Classen, Joseph and Neely, G.
                      Gregory and Richter, Angelika and Penninger, Josef M. and
                      Bechmann, Ingo},
      title        = {{N}euroanatomy of pain-deficiency and cross-modal
                      activation in calcium channel subunit ({CACN}) α2δ3
                      knockout mice},
      journal      = {Brain structure $\&$ function},
      volume       = {223},
      number       = {1},
      issn         = {1863-2661},
      address      = {Berlin},
      publisher    = {Springer},
      reportid     = {FZJ-2018-01232},
      pages        = {111 - 130},
      year         = {2018},
      abstract     = {The phenotype of calcium channel subunit (CACN) α2δ3
                      knockout (KO) mice includes sensory cross-activation and
                      deficient pain perception. Sensory cross-activation defines
                      the activation of a sensory cortical region by input from
                      another modality due to reorganization in the brain such as
                      after sensory loss. To obtain mechanistic insight into both
                      phenomena, we employed a comprehensive battery of
                      neuroanatomical techniques. While CACNα2δ3 was
                      ubiquitously expressed in wild-type mice, it was absent in
                      α2δ3 KO animals. Immunostaining of α1A, α1B, and α1E
                      revealed upregulation of N-type and R-type, but not P/Q-type
                      Cav2 channels in cortical neurons of CACNα2δ3 KO mice.
                      Compared to wild-type mice, axonal processes in
                      somatosensory cortex were enhanced, and dendritic processes
                      reduced, in CACNα2δ3 KO mice. Immunohistochemical and MRI
                      analyses, investigating morphology, thalamocortical and
                      intra-/intercortical trajectories, revealed a disparity
                      between projection and commissural fibers with reduction of
                      the number of spatial specificity of thalamocortical
                      projections. L1cam staining revealed wide-ranging
                      projections of thalamocortical fibers reaching both
                      somatosensory/motor and visual cortical areas. Activation
                      (c-fos+) of excitatory and inhibitory neurons suggested that
                      deficient pain perception in α2δ3 KO mice is unlikely to
                      result from cortical disinhibition. Collectively, our data
                      demonstrate that knock out of CACN α2δ3 results in some
                      structural abnormalities whose functional implications
                      converge to dedifferentiation of sensory activation.},
      cin          = {INM-4 / JARA-BRAIN},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-4-20090406 / $I:(DE-82)080010_20140620$},
      pnm          = {573 - Neuroimaging (POF3-573)},
      pid          = {G:(DE-HGF)POF3-573},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28733833},
      UT           = {WOS:000422845500010},
      doi          = {10.1007/s00429-017-1473-4},
      url          = {https://juser.fz-juelich.de/record/843663},
}