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Ischemia opens neuronal gap junction hemichannels.

Roger J Thompson·Ning Zhou·Brian A MacVicar
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Abstract

Neuronal excitotoxicity during stroke is caused by activation of unidentified large-conductance channels, leading to swelling and calcium dysregulation. We show that ischemic-like conditions [O(2)/glucose deprivation (OGD)] open hemichannels, or half gap junctions, in neurons. Hemichannel opening was indicated by a large linear current and flux across the membrane of small fluorescent molecules. Single-channel openings of hemichannels (530 picosiemens) were observed in OGD. Both the current and dye flux were blocked by inhibitors of hemichannels. Therefore, hemichannel opening contributes to the profound ionic dysregulation during stroke and may be a ubiquitous component of ischemic neuronal death.

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Adenosine TriphosphateAnimalsBrain IschemiaCarbenoxoloneCell HypoxiaCell Membrane PermeabilityConnexinsFluoresceinsGap JunctionsGlucoseHippocampusIn Vitro TechniquesIon ChannelsLanthanumMembrane PotentialsMiceNecrosisNerve Tissue ProteinsNeuronsPatch-Clamp TechniquesRatsRats, WistarRhodaminesStrokeJournal ArticleResearch Support, Non-U.S. Gov't

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Roger J Thompson, Ning Zhou, Brian A MacVicar. 2006-05-12. Ischemia opens neuronal gap junction hemichannels.. https://doi.org/10.1126/science.1126241

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