ArticlePloS one2013
Modulation of TRESK background K+ channel by membrane stretch.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Mechanosensitive receptors in migraine: a systematic review.The journal of headache and pain · 2024Pooled it
- The research progress into cellular mechanosensitive ion channels mediating cancer pain.Channels (Austin, Tex.) · 2025Review
- The potassium channel KNature communications · 2025Article
- Two-Pore Domain Potassium Channel in Neurological Disorders.The Journal of membrane biology · 2021Review
- Development of a novel in vitro assay to screen for neuroprotective drugs against iatrogenic neurite shortening.PloS one · 2021Article
- Proton Sensing on the Ocular Surface: Implications in Eye Pain.Frontiers in pharmacology · 2021Review
- The Background KInternational journal of molecular sciences · 2020Review
- Chloroform is a potent activator of cardiac and neuronal Kir3 channels.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Evolution of acid nociception: ion channels and receptors for detecting acid.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- Anionic Phospholipids Bind to and Modulate the Activity of Human TRESK Background KMolecular neurobiology · 2019Article
- The Role of TRESK in Discrete Sensory Neuron Populations and Somatosensory Processing.Frontiers in molecular neuroscience · 2019Article
- Verapamil Inhibits TRESK (KInternational journal of molecular sciences · 2018Article
- Article
- Effects of analgesics and antidepressants on TREK-2 and TRESK currents.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016Article
- Neuroprotective Effects Against POCD by Photobiomodulation: Evidence from Assembly/Disassembly of the Cytoskeleton.Journal of experimental neuroscience · 2016Review
- Activation of TRESK channels by the inflammatory mediator lysophosphatidic acid balances nociceptive signalling.Scientific reports · 2015Article
- Sensitization of neonatal rat lumbar motoneuron by the inflammatory pain mediator bradykinin.eLife · 2015Article
- THIK-1 (K2P13.1) is a small-conductance background K(+) channel in rat trigeminal ganglion neurons.Pflugers Archiv : European journal of physiology · 2014Article
- Phospholipids that contain polyunsaturated fatty acids enhance neuronal cell mechanics and touch sensation.Cell reports · 2014Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The two-pore domain K(+) channel TRESK is expressed in dorsal root ganglion and trigeminal sensory neurons where it is a major contributor to background K(+) current. TRESK acts as a break to prevent excessive sensory neuron activation and decreases in its expression or function have been involved in neuronal hyperexcitability after injury/inflammation, migraine or altered sensory perception (tingling, cooling and pungent burning sensations). All these effects have implicated this channel in nociception and mechanotransduction. To determine the role of TRESK in sensory transduction, we studied its sensitivity to changes in membrane tension (stretch) in heterologous systems, F-11 cells and trigeminal neurons. Laminar shear stress increased TRESK currents by 22-30%. An increase in membrane tension induced by cell swelling (hypotonic medium) produced a reversible elevation of TRESK currents (39.9%). In contrast, cell shrinkage (hypertonic solution) produced the opposite effect. Membrane crenators or cup-formers produced equivalent effects. In trigeminal sensory neurons, TRESK channels were mechanically stimulated by negative pressure, which led to a 1.51-fold increase in channel open probability. TRESK-like currents in trigeminal neurons were additively inhibited by arachidonic acid, acidic pH and hypertonic stimulation, conditions usually found after tissue inflammation. Our results show that TRESK is modulated by changes in cell membrane tension and/or cell volume. Several key players released during inflammation or tissue injury could modulate sensory neuron activation through small changes in membrane tension.
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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.