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@ARTICLE{Wright:162694,
      author       = {Wright, Sukhvir K and Rosch, Richard E and Wilson, Max A
                      and Upadhya, Manoj A and Dhangar, Divya R and Clarke-Bland,
                      Charlie and Wahid, Tamara T and Barman, Sumanta and Goebels,
                      Norbert and Kreye, Jakob and Prüß, Harald and Jacobson,
                      Leslie and Bassett, Danielle S and Vincent, Angela and
                      Greenhill, Stuart D and Woodhall, Gavin L},
      title        = {{M}ultimodal electrophysiological analyses reveal that
                      reduced synaptic excitatory neurotransmission underlies
                      seizures in a model of {NMDAR} antibody-mediated
                      encephalitis.},
      journal      = {Communications biology},
      volume       = {4},
      number       = {1},
      issn         = {2399-3642},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2021-01351},
      pages        = {1106},
      year         = {2021},
      note         = {CC BY},
      abstract     = {Seizures are a prominent feature in N-Methyl-D-Aspartate
                      receptor antibody (NMDAR antibody) encephalitis, a distinct
                      neuro-immunological disorder in which specific human
                      autoantibodies bind and crosslink the surface of NMDAR
                      proteins thereby causing internalization and a state of
                      NMDAR hypofunction. To further understand ictogenesis in
                      this disorder, and to test a potential treatment compound,
                      we developed an NMDAR antibody mediated rat seizure model
                      that displays spontaneous epileptiform activity in vivo and
                      in vitro. Using a combination of electrophysiological and
                      dynamic causal modelling techniques we show that, contrary
                      to expectation, reduction of synaptic excitatory, but not
                      inhibitory, neurotransmission underlies the ictal events
                      through alterations in the dynamical behaviour of
                      microcircuits in brain tissue. Moreover, in vitro
                      application of a neurosteroid, pregnenolone sulphate, that
                      upregulates NMDARs, reduced established ictal activity. This
                      proof-of-concept study highlights the complexity of circuit
                      disturbances that may lead to seizures and the potential use
                      of receptor-specific treatments in antibody-mediated
                      seizures and epilepsy.},
      keywords     = {Animals / Anti-N-Methyl-D-Aspartate Receptor Encephalitis:
                      chemically induced / Autoantibodies: adverse effects /
                      Disease Models, Animal / Male / Rats / Rats, Wistar /
                      Synaptic Transmission},
      cin          = {AG Prüß},
      ddc          = {570},
      cid          = {I:(DE-2719)1810003},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34545200},
      pmc          = {pmc:PMC8452639},
      doi          = {10.1038/s42003-021-02635-8},
      url          = {https://pub.dzne.de/record/162694},
}