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@ARTICLE{Singh:283184,
      author       = {Singh, Jeet Bahadur and Perelló-Amorós, Bartomeu and
                      Schneeberg, Jenny and Mirzapourdelavar, Hadi and
                      Seidenbecher, Constanze I and Fejtová, Anna and Dityatev,
                      Alexander and Frischknecht, Renato},
      title        = {{A}ctivity-dependent extracellular proteolytic cascade
                      cleaves the {ECM} component brevican to promote structural
                      plasticity.},
      journal      = {EMBO reports},
      volume       = {27},
      number       = {1},
      issn         = {1469-221X},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DZNE-2026-00063},
      pages        = {163 - 185},
      year         = {2026},
      abstract     = {The brain's perineuronal extracellular matrix (ECM) is a
                      crucial factor in maintaining the stability of mature brain
                      circuitry. However, how activity-induced synaptic plasticity
                      is achieved in the adult brain with a dense ECM is unclear.
                      We hypothesized that neuronal activity induces cleavage of
                      ECM, creating conditions for synaptic rearrangements. To
                      test this hypothesis, we investigated neuronal
                      activity-dependent proteolytic cleavage of brevican, a
                      prototypical ECM proteoglycan, and the importance of this
                      process for functional and structural synaptic plasticity in
                      the rat hippocampus ex vivo. Our findings reveal that
                      chemical long-term potentiation (cLTP) triggers rapid
                      brevican cleavage in perisynaptic regions through the
                      activation of an extracellular proteolytic cascade involving
                      proprotein convertases and ADAMTS-4 and ADAMTS-5. This
                      process requires NMDA receptor activation and involves
                      astrocytes. Interfering with cLTP-induced brevican cleavage
                      prevents the formation of new dendritic protrusions in CA1
                      but does not impact LTP induction by theta-burst stimulation
                      of CA3-CA1 synapses. Our data reveal a mechanism of
                      activity-dependent ECM remodeling and suggest that ECM
                      degradation is essential for structural synaptic
                      plasticity.},
      keywords     = {Animals / Brevican: metabolism / Extracellular Matrix:
                      metabolism / Rats / Neuronal Plasticity / Long-Term
                      Potentiation / Proteolysis / Astrocytes: metabolism /
                      Hippocampus: metabolism / Hippocampus: physiology / Male /
                      Synapses: metabolism / Receptors, N-Methyl-D-Aspartate:
                      metabolism / Neurons: metabolism / ADAMTS (Other) / Aggrecan
                      (Other) / Dendritic Spines (Other) / Perineuronal Nets
                      (Other) / Proprotein Convertase (Other) / Brevican (NLM
                      Chemicals) / Receptors, N-Methyl-D-Aspartate (NLM
                      Chemicals)},
      cin          = {AG Dityatev},
      ddc          = {570},
      cid          = {I:(DE-2719)1310007},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41261283},
      doi          = {10.1038/s44319-025-00644-w},
      url          = {https://pub.dzne.de/record/283184},
}