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@ARTICLE{Rhnert:136376,
      author       = {Röhnert, Peter and Schröder, Ulrich H and Ziabreva, Iryna
                      and Täger, Michael and Reymann, Klaus G and Striggow,
                      Frank},
      title        = {{I}nsufficient endogenous redox buffer capacity may
                      underlie neuronal vulnerability to cerebral ischemia and
                      reperfusion.},
      journal      = {Journal of neuroscience research},
      volume       = {90},
      number       = {1},
      issn         = {0360-4012},
      address      = {New York, NY [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {DZNE-2020-02698},
      pages        = {193-202},
      year         = {2012},
      abstract     = {Reactive oxygen species (ROS) are key players in
                      ischemia-induced neurodegeneration. We investigated whether
                      hippocampal neurons may lack sufficient redox-buffering
                      capacity to protect against ROS attacks. Using organotypic
                      hippocampal slice cultures (OHSCs) transiently exposed to
                      oxygen and glucose deprivation (OGD) and gerbils suffering
                      from a two-vessel occlusion (2VO) as complementary ex vivo
                      and in vivo models, we have elucidated whether the intrinsic
                      redox systems interfere with ischemia-induced
                      neurodegeneration. Cell- type-specific immunohistological
                      staining of hippocampal slice cultures revealed that
                      pyramidal neurons, in contrast to astrocytes and microglia,
                      express free thiols only weakly. In addition, free thiol
                      levels were extensively decreased throughout the hippocampal
                      formation immediately after OGD, but recovered within 24 hr
                      after reperfusion. In parallel, progressive glia activation
                      and proliferation were observed. Increased neuronal exposure
                      to ROS was monitored by dihydroethidium oxidation in
                      hippocampal pyramidal cell layers immediately after OGD.
                      Coadministration of reduction equivalents (α-lipoic acid)
                      and thiol-stimulating agents (enalapril, ambroxol) decreased
                      ischemia-induced neuronal damage in OGD-treated OHSCs and in
                      gerbils exposed to 2VO, whereas single drug applications
                      remained ineffective. In summary, limited redox buffering
                      capacities of pyramidal neurons may underlie their
                      exceptional vulnerability to cerebral ischemia.
                      Consistently, multidrug treatments supporting endogenous
                      redox systems may offer a strategy to promote valid
                      neuroprotection.},
      keywords     = {Animals / Brain Ischemia: pathology / Cell Death / Disease
                      Models, Animal / Ethidium: analogs $\&$ derivatives /
                      Ethidium: metabolism / Fluoresceins: metabolism /
                      Gerbillinae / Glial Fibrillary Acidic Protein: metabolism /
                      Glucose: deficiency / Glycoproteins: metabolism /
                      Hippocampus: cytology / Hypoxia / Lectins: metabolism /
                      Neurons: drug effects / Neurons: metabolism / Neurons:
                      pathology / Neuroprotective Agents: pharmacology / Organ
                      Culture Techniques / Oxidation-Reduction / Rats / Rats,
                      Wistar / Reactive Oxygen Species / Reperfusion Injury:
                      pathology / Rhodamines: metabolism / Sulfhydryl Compounds:
                      metabolism / Thioctic Acid: pharmacology /
                      (((4-chloromethyl)benzoyl)amino)-tetramethylrhodamine (NLM
                      Chemicals) / Fluoresceins (NLM Chemicals) / Glial Fibrillary
                      Acidic Protein (NLM Chemicals) / Glycoproteins (NLM
                      Chemicals) / Lectins (NLM Chemicals) / Neuroprotective
                      Agents (NLM Chemicals) / Reactive Oxygen Species (NLM
                      Chemicals) / Rhodamines (NLM Chemicals) / Sulfhydryl
                      Compounds (NLM Chemicals) / isolectin B4-binding
                      glycoprotein, rat (NLM Chemicals) / dihydroethidium (NLM
                      Chemicals) / 5-chloromethylfluorescein (NLM Chemicals) /
                      Thioctic Acid (NLM Chemicals) / Ethidium (NLM Chemicals) /
                      Glucose (NLM Chemicals)},
      cin          = {AG Striggow},
      ddc          = {570},
      cid          = {I:(DE-2719)5000045},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:21971686},
      doi          = {10.1002/jnr.22754},
      url          = {https://pub.dzne.de/record/136376},
}