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@ARTICLE{Grtz:3798,
      author       = {Görtz, P. and Opatz, J. and Siebler, M. and Funke, S. A.
                      and Willbold, D. and Lange-Asschenfeldt, C.},
      title        = {{T}ransient reduction of spontaneous neuronal network
                      activity by sublethal amyloid ß (1-42) peptide
                      concentrations},
      journal      = {Journal of neural transmission / Parkinson's disease and
                      dementia section},
      volume       = {116},
      issn         = {0936-3076},
      address      = {Wien [u.a.]},
      publisher    = {Springer},
      reportid     = {PreJuSER-3798},
      pages        = {351 - 355},
      year         = {2009},
      note         = {This study was supported by a grant from the Stiftung fur
                      Altersforschung (Age Research Foundation) of the
                      Heinrich-Heine-Universitat Dusseldorf (C. L.-A. and P. G.).},
      abstract     = {Soluble amyloid beta(1-42) (A beta(1-42)) peptide has
                      recently been assigned a key role in early Alzheimer's
                      disease (AD) pathophysiology accounting for synaptic
                      dysfunction before amyloid plaque formation and
                      neurodegeneration can occur. Following sublethal A
                      beta(1-42) administration, we observed an acute but
                      transient reduction of the spike and burst rate of
                      spontaneously active cortical networks cultured on
                      microelectrode arrays. This simple experimental system
                      appears suitable for future long-term pharmacological and
                      genetic studies of A beta(1-42) signaling, thus providing a
                      valuable new tool in AD research.},
      keywords     = {Action Potentials: drug effects / Action Potentials:
                      physiology / Amyloid beta-Peptides: administration $\&$
                      dosage / Amyloid beta-Peptides: metabolism / Amyloid
                      beta-Peptides: pharmacology / Animals / Cell Culture
                      Techniques / Cerebral Cortex: cytology / Electrophysiology /
                      Microelectrodes / Nerve Net: drug effects / Nerve Net:
                      physiology / Neurons: drug effects / Neurons: physiology /
                      Peptide Fragments: administration $\&$ dosage / Peptide
                      Fragments: metabolism / Peptide Fragments: pharmacology /
                      Rats / Amyloid beta-Peptides (NLM Chemicals) / Peptide
                      Fragments (NLM Chemicals) / amyloid beta-protein (1-42) (NLM
                      Chemicals) / J (WoSType)},
      cin          = {ISB-3 / JARA-HPC},
      ddc          = {610},
      cid          = {I:(DE-Juel1)VDB942 / $I:(DE-82)080012_20140620$},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Clinical Neurology / Neurosciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:19214376},
      UT           = {WOS:000263897900011},
      doi          = {10.1007/s00702-009-0188-y},
      url          = {https://juser.fz-juelich.de/record/3798},
}