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@ARTICLE{Nascimento:273977,
      author       = {Nascimento, Filipe and Özyurt, M Görkem and Halablab,
                      Kareen and Bhumbra, Gardave Singh and Caron, Guillaume and
                      Bączyk, Marcin and Zytnicki, Daniel and Manuel, Marin and
                      Roselli, Francesco and Brownstone, Rob and Beato, Marco},
      title        = {{S}pinal microcircuits go through multiphasic homeostatic
                      compensations in a mouse model of motoneuron degeneration.},
      journal      = {Cell reports},
      volume       = {43},
      number       = {12},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2024-01426},
      pages        = {115046},
      year         = {2024},
      abstract     = {In many neurological conditions, early-stage neural circuit
                      adaptation preserves relatively normal behavior. In some
                      diseases, spinal motoneurons progressively degenerate yet
                      movement remains initially preserved. This study
                      investigates whether these neurons and associated
                      microcircuits adapt in a mouse model of progressive
                      motoneuron degeneration. Using a combination of in vitro and
                      in vivo electrophysiology and super-resolution microscopy,
                      we find that, early in the disease, neurotransmission in a
                      key pre-motor circuit, the recurrent inhibition mediated by
                      Renshaw cells, is reduced by half due to impaired quantal
                      size associated with decreased glycine receptor density.
                      This impairment is specific and not a widespread feature of
                      spinal inhibitory circuits. Furthermore, it recovers at
                      later stages of disease. Additionally, an increased
                      probability of release from proprioceptive afferents leads
                      to increased monosynaptic excitation of motoneurons. We
                      reveal that, in this motoneuron degenerative condition,
                      spinal microcircuits undergo specific multiphasic
                      homeostatic compensations that may contribute to
                      preservation of force output.},
      keywords     = {Animals / Motor Neurons: metabolism / Motor Neurons:
                      pathology / Mice / Homeostasis / Disease Models, Animal /
                      Spinal Cord: pathology / Spinal Cord: metabolism / Synaptic
                      Transmission: physiology / Receptors, Glycine: metabolism /
                      Nerve Degeneration: pathology / Mice, Inbred C57BL / Renshaw
                      Cells: metabolism / ALS (Other) / CP: Cell biology (Other) /
                      CP: Neuroscience (Other) / Renshaw cells (Other) /
                      electrophysiology (Other) / glycine receptors (Other) /
                      motoneurons (Other) / motor control (Other) / quantal
                      analysis (Other) / sensory afferents (Other) / spinal cord
                      (Other)},
      cin          = {AG Roselli},
      ddc          = {610},
      cid          = {I:(DE-2719)1910001},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39656589},
      doi          = {10.1016/j.celrep.2024.115046},
      url          = {https://pub.dzne.de/record/273977},
}