ArticleThe Journal of physiology2005
The lipid-activated two-pore domain K+ channel TREK-1 is resistant to hypoxia: implication for ischaemic neuroprotection.
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 29 papers.
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Who cites it
29 citing papers in PubMed, 60 citations in OpenAlex.
- Lipid Regulation of Mechanosensitive Ion Channels.International journal of molecular sciences · 2026Review
- Effect of two activators on the gating of a KBiophysical journal · 2024Article
- 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
- Identification and characterization of two zebrafish Twik related potassium channels, Kcnk2a and Kcnk2b.Scientific reports · 2018Article
- TREK-1 mediates isoflurane-induced cytotoxicity in astrocytes.BMC anesthesiology · 2017Article
- Fluoxetine Protection in Decompression Sickness in Mice is Enhanced by Blocking TREK-1 Potassium Channel with the "spadin" Antidepressant.Frontiers in physiology · 2016Article
- Fatty Acid Regulation of Voltage- and Ligand-Gated Ion Channel Function.Frontiers in physiology · 2016Review
- Ischaemic concentrations of lactate increase TREK1 channel activity by interacting with a single histidine residue in the carboxy terminal domain.The Journal of physiology · 2016Article
- In vitro and in vivo regulation of synaptogenesis by the novel antidepressant spadin.British journal of pharmacology · 2015Article
- TASK channels in arterial chemoreceptors and their role in oxygen and acid sensing.Pflugers Archiv : European journal of physiology · 2015Review
- The CNS under pathophysiologic attack--examining the role of K₂p channels.Pflugers Archiv : European journal of physiology · 2015Review
- Linolenic acid provides multi-cellular protective effects after photothrombotic cerebral ischemia in rats.Neurochemical research · 2014Article
- Involvement of TREK-1 activity in astrocyte function and neuroprotection under simulated ischemia conditions.Journal of molecular neuroscience : MN · 2013Article
- The human carotid body transcriptome with focus on oxygen sensing and inflammation--a comparative analysis.The Journal of physiology · 2012Article
- Changes in lipid-sensitive two-pore domain potassium channel TREK-1 expression and its involvement in astrogliosis following cerebral ischemia in rats.Journal of molecular neuroscience : MN · 2012Article
- Peripheral chemoreceptors: function and plasticity of the carotid body.Comprehensive Physiology · 2012Review
- Behavioral characterization of mice lacking Trek channels.Frontiers in behavioral neuroscience · 2012Article
- Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TREK-1 is a member of the two-pore domain potassium (K(2P)) channel family that is mechano-, heat, pH, voltage and lipid sensitive. It is highly expressed in the central nervous system and probably encodes one of the previously described arachidonic acid-activated K(+) channels. Polyunsaturated fatty acids and lysophospholipids protect the brain against global ischaemia. Since both lipids are openers of TREK-1, it has been suggested that this K(2P) channel is directly involved in neuroprotection. Recently, however, this view has been challenged by a report claiming that TREK-1 and its activation by arachidonic acid is inhibited by hypoxia. In the present study, we demonstrate that the bubbling of saline with gases results in the loss of arachidonic acid from solution. Using experimental conditions which obviate this experimental artefact we demonstrate that TREK-1 is resistant to hypoxia and is strongly activated by arachidonic acid even at low P(O(2)) (< 4 Torr). Furthermore, hypoxia fails to affect basal as well as 2,4,6-trinitrophenol- and acid-stimulated TREK-1 currents. These data are supportive for a possible role of TREK-1 in ischaemic neuroprotection and in cell signalling via arachidonic acid.
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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.