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@ARTICLE{Matuszko:139241,
      author       = {Matuszko, Gabriela and Curreli, Sebastiano and Kaushik,
                      Rahul and Becker, Axel and Dityatev, Alexander},
      title        = {{E}xtracellular matrix alterations in the ketamine model of
                      schizophrenia.},
      journal      = {Neuroscience},
      volume       = {350},
      issn         = {0306-4522},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DZNE-2020-05563},
      pages        = {13-22},
      year         = {2017},
      abstract     = {The neural extracellular matrix (ECM) plays an important
                      role in regulation of perisomatic GABAergic inhibition and
                      synaptic plasticity in the hippocampus and cortex. Decreased
                      labeling of perineuronal nets, a form of ECM predominantly
                      associated with parvalbumin-expressing interneurons in the
                      brain, has been observed in post-mortem studies of
                      schizophrenia patients, specifically, in brain areas such as
                      prefrontal cortex, entorhinal cortex, and amygdala.
                      Moreover, glial ECM in the form of dandelion clock-like
                      structures was reported to be altered in schizophrenia
                      patients. Here, we verified whether similar abnormalities in
                      neural ECM can be reproduced in a rat model of
                      schizophrenia, in which animals received sub-chronic
                      administration of ketamine to reproduce the aspects of
                      disease related to disrupted signaling through
                      N-methyl-D-aspartate receptors. Our study focused on two
                      schizophrenia-related brain areas, namely the medial
                      prefrontal cortex (mPFC) and hippocampus. Semi-quantitative
                      immunohistochemistry was performed to evaluate investigate
                      ECM expression using Wisteria floribunda agglutinin (WFA)
                      and CS56 antibody, both labeling distinct chondroitin
                      sulfate epitopes enriched in perineuronal nets and glial
                      ECM, respectively. Our analysis revealed that
                      ketamine-treated rats exhibit reduced number of WFA-labeled
                      perineuronal nets, and a decreased intensity of parvalbumin
                      fluorescence in mPFC interneurons somata. Moreover, we found
                      an increased expression of CS56 immunoreactive form of ECM.
                      Importantly, the loss of perineuronal nets was revealed in
                      the mPFC, and was not detected in the hippocampus,
                      suggesting regional specificity of ECM alterations. These
                      data open an avenue for further investigations of functional
                      importance of ECM abnormalities in schizophrenia as well as
                      for search of treatments for their compensation.},
      keywords     = {Amygdala: drug effects / Amygdala: metabolism / Animals /
                      Disease Models, Animal / Extracellular Matrix: drug effects
                      / Extracellular Matrix: metabolism / Hippocampus: drug
                      effects / Hippocampus: metabolism / Immunohistochemistry:
                      methods / Ketamine: pharmacology / Male / Neuroglia: drug
                      effects / Neuroglia: metabolism / Neurons: drug effects /
                      Neurons: metabolism / Parvalbumins: metabolism / Rats,
                      Sprague-Dawley / Schizophrenia: chemically induced /
                      Schizophrenia: metabolism / Parvalbumins (NLM Chemicals) /
                      Ketamine (NLM Chemicals)},
      cin          = {AG Dityatev / Core Technical Staff},
      ddc          = {610},
      cid          = {I:(DE-2719)1310007 / I:(DE-2719)1340007},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28323012},
      doi          = {10.1016/j.neuroscience.2017.03.010},
      url          = {https://pub.dzne.de/record/139241},
}