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@ARTICLE{Klin:140045,
      author       = {Kälin, Stefanie and Miller, Kelly R and Kälin, Roland E
                      and Jendrach, Marina and Witzel, Christian and Heppner,
                      Frank L},
      title        = {{CNS} myeloid cells critically regulate heat hyperalgesia.},
      journal      = {The journal of clinical investigation},
      volume       = {128},
      number       = {7},
      issn         = {0021-9738},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DZNE-2020-06367},
      pages        = {2774-2786},
      year         = {2018},
      abstract     = {Activation of non-neuronal microglia is thought to play a
                      causal role in spinal processing of neuropathic pain. To
                      specifically investigate microglia-mediated effects in a
                      model of neuropathic pain and overcome the methodological
                      limitations of previous approaches exploring microglia
                      function upon nerve injury, we selectively ablated resident
                      microglia by intracerebroventricular ganciclovir infusion
                      into male CD11b-HSVTK-transgenic mice, which was followed by
                      a rapid, complete, and persistent (23 weeks) repopulation of
                      the CNS by peripheral myeloid cells. In repopulated mice
                      that underwent sciatic nerve injury, we observed a normal
                      response to mechanical stimuli, but an absence of thermal
                      hypersensitivity ipsilateral to the injured nerve.
                      Furthermore, we found that neuronal expression of calcitonin
                      gene-related peptide (CGRP), which is a marker of neurons
                      essential for heat responses, was diminished in the dorsal
                      horn of the spinal cord in repopulated mice. These findings
                      identify distinct mechanisms for heat and mechanical
                      hypersensitivity and highlight a crucial contribution of CNS
                      myeloid cells in the facilitation of noxious heat.},
      keywords     = {Animals / Calcitonin Gene-Related Peptide: physiology /
                      Central Nervous System: pathology / Central Nervous System:
                      physiopathology / Hot Temperature / Hyperalgesia: pathology
                      / Hyperalgesia: physiopathology / Male / Mice / Mice, Inbred
                      C57BL / Mice, Transgenic / Microglia: cytology / Microglia:
                      physiology / Myeloid Cells: pathology / Myeloid Cells:
                      physiology / Neuralgia: pathology / Neuralgia:
                      physiopathology / Peptide Fragments: physiology / Peripheral
                      Nerve Injuries: pathology / Peripheral Nerve Injuries:
                      physiopathology / Peripheral Nerves: pathology / Peripheral
                      Nerves: physiopathology / Spinal Cord Dorsal Horn: pathology
                      / Spinal Cord Dorsal Horn: physiopathology / Peptide
                      Fragments (NLM Chemicals) / calcitonin gene related peptide
                      (1-7) (NLM Chemicals) / Calcitonin Gene-Related Peptide (NLM
                      Chemicals)},
      cin          = {AG Heppner},
      ddc          = {610},
      cid          = {I:(DE-2719)1810007},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29634489},
      pmc          = {pmc:PMC6025970},
      doi          = {10.1172/JCI95305},
      url          = {https://pub.dzne.de/record/140045},
}