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@ARTICLE{Hasan:143651,
      author       = {M. T. Hasan and F. Althammer$^*$ and M. Silva da
                      Gouveia$^*$ and S. Goyon and M. Eliava$^*$ and A.
                      Lefevre$^*$ and D. Kerspern and J. Schimmer$^*$ and A.
                      Raftogianni$^*$ and J. Wahis and H. S. Knobloch-Bollmann$^*$
                      and Y. Tang$^*$ and X. Liu$^*$ and A. Jain$^*$ and V.
                      Chavant and Y. Goumon and J.-M. Weislogel and R. Hurlemann
                      and S. C. Herpertz and C. Pitzer and P. Darbon and G. K.
                      Dogbevia and I. Bertocchi and M. E. Larkum and R. Sprengel
                      and H. Bading and A. Charlet and V. Grinevich$^*$},
      title        = {{A} {F}ear {M}emory {E}ngram and {I}ts {P}lasticity in the
                      {H}ypothalamic {O}xytocin {S}ystem.},
      journal      = {Neuron},
      volume       = {103},
      number       = {1},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2019-01225},
      pages        = {133-146.e8},
      year         = {2019},
      abstract     = {Oxytocin (OT) release by axonal terminals onto the central
                      nucleus of the amygdala exerts anxiolysis. To investigate
                      which subpopulation of OT neurons contributes to this
                      effect, we developed a novel method: virus-delivered genetic
                      activity-induced tagging of cell ensembles (vGATE). With the
                      vGATE method, we identified and permanently tagged a small
                      subpopulation of OT cells, which, by optogenetic
                      stimulation, strongly attenuated contextual fear-induced
                      freezing, and pharmacogenetic silencing of tagged OT neurons
                      impaired context-specific fear extinction, demonstrating
                      that the tagged OT neurons are sufficient and necessary,
                      respectively, to control contextual fear. Intriguingly, OT
                      cell terminals of fear-experienced rats displayed enhanced
                      glutamate release in the amygdala. Furthermore, rats exposed
                      to another round of fear conditioning displayed 5-fold more
                      activated magnocellular OT neurons in a novel environment
                      than a familiar one, possibly for a generalized fear
                      response. Thus, our results provide first evidence that
                      hypothalamic OT neurons represent a fear memory engram.},
      cin          = {V078},
      ddc          = {610},
      cid          = {I:(DE-He78)V078-20160331},
      pnm          = {319H - Addenda (POF3-319H)},
      pid          = {G:(DE-HGF)POF3-319H},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31104950},
      doi          = {10.1016/j.neuron.2019.04.029},
      url          = {https://inrepo02.dkfz.de/record/143651},
}