% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Hilton:163651,
      author       = {Hilton, Brett J and Husch, Andreas and Schaffran, Barbara
                      and Lin, Tien-Chen and Burnside, Emily R and Dupraz,
                      Sebastian and Schelski, Max and Kim, Jisoo and Müller,
                      Johannes Alexander and Schoch, Susanne and Imig, Cordelia
                      and Brose, Nils and Bradke, Frank},
      title        = {{A}n active vesicle priming machinery suppresses axon
                      regeneration upon adult {CNS} injury.},
      journal      = {Neuron},
      volume       = {110},
      number       = {1},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2022-00397},
      pages        = {51 - 69.e7},
      year         = {2022},
      note         = {(CC BY-NC-ND)},
      abstract     = {Axons in the adult mammalian central nervous system fail to
                      regenerate after spinal cord injury. Neurons lose their
                      capacity to regenerate during development, but the
                      intracellular processes underlying this loss are unclear. We
                      found that critical components of the presynaptic active
                      zone prevent axon regeneration in adult mice. Transcriptomic
                      analysis combined with live-cell imaging revealed that adult
                      primary sensory neurons downregulate molecular constituents
                      of the synapse as they acquire the ability to rapidly grow
                      their axons. Pharmacogenetic reduction of neuronal
                      excitability stimulated axon regeneration after adult spinal
                      cord injury. Genetic gain- and loss-of-function experiments
                      uncovered that essential synaptic vesicle priming proteins
                      of the presynaptic active zone, but not
                      clostridial-toxin-sensitive VAMP-family SNARE proteins,
                      inhibit axon regeneration. Systemic administration of
                      Baclofen reduced voltage-dependent Ca2+ influx in primary
                      sensory neurons and promoted their regeneration after spinal
                      cord injury. These findings indicate that functional
                      presynaptic active zones constitute a major barrier to axon
                      regeneration.},
      keywords     = {Animals / Axons: metabolism / Central Nervous System:
                      metabolism / Mammals / Mice / Nerve Regeneration: physiology
                      / Neurons: metabolism / Spinal Cord Injuries: metabolism /
                      Baclofen (Other) / Munc13 (Other) / RIM1/2 (Other) / active
                      zone (Other) / axon injury (Other) / axon regeneration
                      (Other) / spinal cord injury (Other)},
      cin          = {AG Bradke},
      ddc          = {610},
      cid          = {I:(DE-2719)1013002},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34706221},
      pmc          = {pmc:PMC8730507},
      doi          = {10.1016/j.neuron.2021.10.007},
      url          = {https://pub.dzne.de/record/163651},
}