ArticleThe Journal of physiology2005
The effects of hypoxia on the modulation of human TREK-1 potassium channels.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Carotid body chemoreceptors: physiology, pathology, and implications for health and disease.Physiological reviews · 2021Review
- Intracellular activation of full-length human TREK-1 channel by hypoxia, high lactate, and low pH denotes polymodal integration by ischemic factors.Pflugers Archiv : European journal of physiology · 2021Article
- Tandem pore TWIK-related potassium channels and neuroprotection.Neural regeneration research · 2019Review
- The CNS under pathophysiologic attack--examining the role of K₂p channels.Pflugers Archiv : European journal of physiology · 2015Review
- TREK-1 currents in smooth muscle cells from pregnant human myometrium.American journal of physiology. Cell physiology · 2013Article
- Behavioral characterization of mice lacking Trek channels.Frontiers in behavioral neuroscience · 2012Article
- Novel neuroprotectant chiral 3-n-butylphthalide inhibits tandem-pore-domain potassium channel TREK-1.Acta pharmacologica Sinica · 2011Article
- A human TREK-1/HEK cell line: a highly efficient screening tool for drug development in neurological diseases.PloS one · 2011Article
- AMP-activated protein kinase inhibits TREK channels.The Journal of physiology · 2009Article
- The Inhibition of TREK2 Channel by an Oxidizing Agent, 5,5'-dithio-bis (2-nitrobenzoic acid), via Interaction with the C-terminus Distal to the 353rd Amino Acid.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2008Article
- K+ channels in apoptosis.The Journal of membrane biology · 2006Review
- Analyses of gating thermodynamics and effects of deletions in the mechanosensitive channel TREK-1: comparisons with structural models.Channels (Austin, Tex.)Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two-pore-domain potassium channels are a family of ion channels that are widely believed to play an important role in maintaining and regulating neuronal excitability. It has been shown that they can be modulated by an extraordinarily diverse range of endogenous and exogenous factors. One particular member of the family, TREK-1 (also known as KCNK2), is activated by increasing temperature, membrane stretch and internal acidosis, but is also sensitive to the presence of certain polyunsaturated fatty acids (such as arachidonic acid), neuroprotectants (such as riluzole) and volatile and gaseous general anaesthetics (such as halothane and nitrous oxide). It has recently been reported that TREK-1 channels are also affected by oxygen concentrations, and that at the levels of hypoxia that occur in the normal human brain, the channels greatly change their properties and, for example, lose their ability to be modulated by arachidonic acid and internal acidosis. These reports seriously challenge the idea that TREK-1 is a target for general anaesthetics and neuroprotectants. However, in this report we show that TREK-1 is not oxygen sensitive, and its ability to be activated by anaesthetics, arachidonic acid and internal acidosis remains unaltered under conditions of hypoxia. We further show that the protocol used by previous workers to prepare hypoxic solutions of arachidonic acid results in the removal of the compound from solution.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.