ArticlePflugers Archiv : European journal of physiology2003
Effect of acute hypoxia on ATP-sensitive potassium currents in substantia gelatinosa neurons of juvenile rats.
Article in Pflugers Archiv : European journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- A lab-on-a-chip for hypoxic patch clamp measurements combined with optical tweezers and spectroscopy- first investigations of single biological cells.Biomedical engineering online · 2015Article
- Ionic storm in hypoxic/ischemic stress: can opioid receptors subside it?Progress in neurobiology · 2010Review
- Hypoxia-induced changes in neuronal network properties.Molecular neurobiology · 2005Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although hypoxia is known to affect membrane excitability of various neurons by various mechanisms, the effects of hypoxia on substantia gelatinosa (SG) neurons have not yet been elucidated. In whole-cell or perforated patch-clamp recordings from SG neurons, we showed that acute hypoxia induces a reversible hyperpolarization of -6.1+/-1.3 mV of the resting membrane potential and an outwards current of 9.48+/-1.71 pA at a holding potential of -60 mV. The reversal potentials of the hypoxia-induced current depended on [K(+)](o). The hypoxia-induced hyperpolarization and outwards current were abolished completely by BaCl(2), but not by CsCl. Glibenclamide, a blocker of K(ATP) channels, blocked the hypoxia-induced hyperpolarization. Pretreatment with cromakalim, an opener of K(ATP) channels, occluded the hypoxia-induced hyperpolarization. Any alteration by hypoxia was not observed in the presence of an internal solution with a high [ATP] (10 mM). The above results suggest that hypoxia-induced hyperpolarization in SG neurons is mediated by activation of K(ATP) channels.
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