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@ARTICLE{Braun:283561,
      author       = {Braun, Ramona and Klein, Rebecca and Walter, Helene Luise
                      and Ohren, Maurice and Freudenmacher, Lars and Getachew,
                      Kaleab and Ladwig, Anne and Luelling, Joachim and Neumaier,
                      Bernd and Endepols, Heike and Graf, Rudolf and Hoehn,
                      Mathias and Fink, Gereon Rudolf and Schroeter, Michael and
                      Rueger, Maria Adele},
      title        = {{T}ranscranial direct current stimulation accelerates
                      recovery of function, induces neurogenesis and recruits
                      oligodendrocyte precursors in a rat model of stroke},
      journal      = {Experimental neurology},
      volume       = {279},
      issn         = {0014-4886},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {FZJ-2016-01876},
      pages        = {127 - 136},
      year         = {2016},
      abstract     = {BackgroundClinical data suggest that transcranial direct
                      current stimulation (tDCS) may be used to facilitate
                      rehabilitation after stroke. However, data are inconsistent
                      and the neurobiological mechanisms underlying tDCS remain
                      poorly explored, impeding its implementation into clinical
                      routine. In the healthy rat brain, tDCS affects neural stem
                      cells (NSC) and microglia. We here investigated whether tDCS
                      applied after stroke also beneficially affects these cells,
                      which are known to be involved in regeneration and
                      repair.MethodsFocal cerebral ischemia was induced in rats by
                      transient occlusion of the middle cerebral artery.
                      Twenty-eight animals with comparable infarcts, as judged by
                      magnetic resonance imaging, were randomized to receive a
                      multi-session paradigm of either cathodal, anodal, or sham
                      tDCS. Behaviorally, recovery of motor function was assessed
                      by Catwalk. Proliferation in the NSC niches was monitored by
                      Positron-Emission-Tomography (PET) employing the radiotracer
                      3′-deoxy-3′-[18F]fluoro-l-thymidine ([18F]FLT).
                      Microglia activation was depicted with [11C]PK11195-PET. In
                      addition, immunohistochemical analyses were used to quantify
                      neuroblasts, oligodendrocyte precursors, and activation and
                      polarization of microglia.ResultsAnodal and cathodal tDCS
                      both accelerated functional recovery, though affecting
                      different aspects of motor function. Likewise, tDCS induced
                      neurogenesis independently of polarity, while only cathodal
                      tDCS recruited oligodendrocyte precursors towards the
                      lesion. Moreover, cathodal stimulation preferably supported
                      M1-polarization of microglia.ConclusionsTDCS acts through
                      multifaceted mechanisms that far exceed its primary
                      neurophysiological effects, encompassing proliferation and
                      migration of stem cells, their neuronal differentiation, and
                      modulation of microglia responses.},
      cin          = {INM-3 / INM-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-5-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572)},
      pid          = {G:(DE-HGF)POF3-572},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000374612900011},
      pubmed       = {pmid:26923911},
      doi          = {10.1016/j.expneurol.2016.02.018},
      url          = {https://juser.fz-juelich.de/record/283561},
}