| Role for nitric oxide in permeability of hippocampal neuronal hemichannels during oxygen glucose deprivation. | |
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MedLine Citation:
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PMID: 18381763 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Increased hemichannel opening induced by oxygen glucose deprivation (OGD) was reported in the hippocampal pyramidal neuron. It was suggested that the pannexin1 hemichannel opening could mediate ionic flux dysregulation, anoxic depolarization, and energy-depleting efflux of glucose and ATP for ischemic neurons. However, the regulatory mechanisms of pannexin1 hemichannel opening have been poorly understood. Here we showed that excessive generation of nitric oxide (NO) during ischemia could induce the calcein leakage from neurons, which was markedly reduced by NO synthase inhibitor. The calcein leakage from neurons during OGD was also attenuated by the application of N-ethylmaleimide (NEM), an SH-alkylating agent, and dithiothreitol (DTT), a reducer of oxidized sulfhydryl groups. However, the soluble guanylyl cyclase (sGC) inhibitor had a minor effect on the calcein leakage during OGD. Furthermore, the elevated intracellular but not extracellular levels of glutathione could also inhibit the calcein leakage during OGD. Similar results were observed in metabolic inhibition (MI), which is another ischemic-like condition. Finally, immunocytochemical and immunoblotting analysis revealed that, after 1 hr of OGD stimulation, the distribution and expression of pannexin1 showed no significant difference compared with control. However, the pannexin1 mRNA expression was elevated after 1 hr of OGD and a sustained increase was maintained during reperfusion. These results implied that the reactive oxygen species (ROS), especially NO, might be involved in the enhanced pannexin1 hemichannel opening and that the S-nitrosylation but not the NO/cGMP pathway played a more important role in this event. |
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Authors:
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Le Zhang; Tongle Deng; Yiguo Sun; Kezhou Liu; Yi Yang; Xiaoxiang Zheng |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of neuroscience research Volume: 86 ISSN: 1097-4547 ISO Abbreviation: J. Neurosci. Res. Publication Date: 2008 Aug |
Date Detail:
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Created Date: 2008-07-16 Completed Date: 2008-09-30 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7600111 Medline TA: J Neurosci Res Country: United States |
Other Details:
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Languages: eng Pagination: 2281-91 Citation Subset: IM |
Affiliation:
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Department of Biomedical Engineering, Key Laboratory of Biomedical Engineering of Ministry of Education, Zhejiang University, Hangzhou, People's Republic of China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blotting, Western Cell Hypoxia / physiology* Cell Membrane Permeability / drug effects, physiology* Connexins / metabolism Cyclic GMP / metabolism Enzyme Inhibitors / pharmacology Fluoresceins / metabolism Fluorescent Dyes / metabolism Glucose / deficiency Hippocampus / drug effects, metabolism* Immunohistochemistry Nerve Tissue Proteins / metabolism Neurons / drug effects, metabolism Nitric Oxide / metabolism* Rats Rats, Sprague-Dawley Reactive Oxygen Species / metabolism Reverse Transcriptase Polymerase Chain Reaction Signal Transduction / drug effects, physiology |
| Chemical | |
Reg. No./Substance:
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0/Connexins; 0/Enzyme Inhibitors; 0/Fluoresceins; 0/Fluorescent Dyes; 0/Nerve Tissue Proteins; 0/Reactive Oxygen Species; 0/pannexin 1, rat; 10102-43-9/Nitric Oxide; 1461-15-0/fluorexon; 50-99-7/Glucose; 7665-99-8/Cyclic GMP |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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