Home > Publications Database > Insufficient endogenous redox buffer capacity may underlie neuronal vulnerability to cerebral ischemia and reperfusion. > print

001     136376
005     20240321220046.0
024 7 _ |a 10.1002/jnr.22754
|2 doi
024 7 _ |a pmid:21971686
|2 pmid
024 7 _ |a 0360-4012
|2 ISSN
024 7 _ |a 1097-4547
|2 ISSN
037 _ _ |a DZNE-2020-02698
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Röhnert, Peter
|0 P:(DE-HGF)0
|b 0
245 _ _ |a Insufficient endogenous redox buffer capacity may underlie neuronal vulnerability to cerebral ischemia and reperfusion.
260 _ _ |a New York, NY [u.a.]
|c 2012
|b Wiley-Liss
264 _ 1 |3 online
|2 Crossref
|b Wiley
|c 2011-10-04
264 _ 1 |3 print
|2 Crossref
|b Wiley
|c 2012-01-01
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1589870591_28441
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a 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.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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|c POF3-342
|f POF III
|x 0
542 _ _ |i 2015-09-01
|2 Crossref
|u http://doi.wiley.com/10.1002/tdm_license_1.1
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a (((4-chloromethyl)benzoyl)amino)-tetramethylrhodamine
|2 NLM Chemicals
650 _ 7 |a Fluoresceins
|2 NLM Chemicals
650 _ 7 |a Glial Fibrillary Acidic Protein
|2 NLM Chemicals
650 _ 7 |a Glycoproteins
|2 NLM Chemicals
650 _ 7 |a Lectins
|2 NLM Chemicals
650 _ 7 |a Neuroprotective Agents
|2 NLM Chemicals
650 _ 7 |a Reactive Oxygen Species
|2 NLM Chemicals
650 _ 7 |a Rhodamines
|2 NLM Chemicals
650 _ 7 |a Sulfhydryl Compounds
|2 NLM Chemicals
650 _ 7 |a isolectin B4-binding glycoprotein, rat
|2 NLM Chemicals
650 _ 7 |a dihydroethidium
|0 104821-25-2
|2 NLM Chemicals
650 _ 7 |a 5-chloromethylfluorescein
|0 136832-63-8
|2 NLM Chemicals
650 _ 7 |a Thioctic Acid
|0 73Y7P0K73Y
|2 NLM Chemicals
650 _ 7 |a Ethidium
|0 EN464416SI
|2 NLM Chemicals
650 _ 7 |a Glucose
|0 IY9XDZ35W2
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Brain Ischemia: pathology
|2 MeSH
650 _ 2 |a Cell Death
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Ethidium: analogs & derivatives
|2 MeSH
650 _ 2 |a Ethidium: metabolism
|2 MeSH
650 _ 2 |a Fluoresceins: metabolism
|2 MeSH
650 _ 2 |a Gerbillinae
|2 MeSH
650 _ 2 |a Glial Fibrillary Acidic Protein: metabolism
|2 MeSH
650 _ 2 |a Glucose: deficiency
|2 MeSH
650 _ 2 |a Glycoproteins: metabolism
|2 MeSH
650 _ 2 |a Hippocampus: cytology
|2 MeSH
650 _ 2 |a Hypoxia
|2 MeSH
650 _ 2 |a Lectins: metabolism
|2 MeSH
650 _ 2 |a Neurons: drug effects
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
650 _ 2 |a Neurons: pathology
|2 MeSH
650 _ 2 |a Neuroprotective Agents: pharmacology
|2 MeSH
650 _ 2 |a Organ Culture Techniques
|2 MeSH
650 _ 2 |a Oxidation-Reduction
|2 MeSH
650 _ 2 |a Rats
|2 MeSH
650 _ 2 |a Rats, Wistar
|2 MeSH
650 _ 2 |a Reactive Oxygen Species
|2 MeSH
650 _ 2 |a Reperfusion Injury: pathology
|2 MeSH
650 _ 2 |a Rhodamines: metabolism
|2 MeSH
650 _ 2 |a Sulfhydryl Compounds: metabolism
|2 MeSH
650 _ 2 |a Thioctic Acid: pharmacology
|2 MeSH
700 1 _ |a Schröder, Ulrich H
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Ziabreva, Iryna
|0 P:(DE-HGF)0
|b 2
700 1 _ |a Täger, Michael
|0 P:(DE-HGF)0
|b 3
700 1 _ |a Reymann, Klaus G
|0 P:(DE-HGF)0
|b 4
700 1 _ |a Striggow, Frank
|0 P:(DE-2719)9000420
|b 5
|e Last author
|u dzne
773 1 8 |a 10.1002/jnr.22754
|b : Wiley, 2011-10-04
|n 1
|p 193-202
|3 journal-article
|2 Crossref
|t Journal of Neuroscience Research
|v 90
|y 2011
|x 0360-4012
773 _ _ |a 10.1002/jnr.22754
|g Vol. 90, no. 1, p. 193 - 202
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|t Journal of neuroscience research
|v 90
|y 2011
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909 C O |o oai:pub.dzne.de:136376
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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|k DZNE
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913 1 _ |a DE-HGF
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