ArticleMolecular medicine reports2012
TRESK gene recombinant adenovirus vector inhibits capsaicin-mediated substance P release from cultured rat dorsal root ganglion neurons.
Article in Molecular medicine reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 35 citations in OpenAlex.
- TRESK Regulates Gm11874 to Induce Apoptosis of Spinal Cord Neurons via ATP5i Mediated Oxidative Stress and DNA Damage.Neurochemical research · 2021Article
- Anionic Phospholipids Bind to and Modulate the Activity of Human TRESK Background KMolecular neurobiology · 2019Article
- Reversal of TRESK Downregulation Alleviates Neuropathic Pain by Inhibiting Activation of Gliocytes in the Spinal Cord.Neurochemical research · 2017Article
- Two-pore domain potassium channels: potential therapeutic targets for the treatment of pain.Pflugers Archiv : European journal of physiology · 2015Review
- Properties, regulation, pharmacology, and functions of the K₂p channel, TRESK.Pflugers Archiv : European journal of physiology · 2015Review
- Article
- Over-expression of TRESK K(+) channels reduces the excitability of trigeminal ganglion nociceptors.PloS one · 2014Article
- Functional analysis of a migraine-associated TRESK K+ channel mutation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- TRESK KeNeuroArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was conducted to determine whether the activation of TRESK in the dorsal root ganglion (DRG) by the TRESK gene recombinant adenovirus vector inhibits the capsaicin-evoked substance P (SP) release using a radioimmunoassay. TRESK is an outwardly rectifying K+ current channel that contributes to the resting potential and is the most important background potassium channel in DRG. Previous studies have shown that neuropathic pain (NP) is closely related to the regulation of certain potassium channels in DRG neurons, while DRG-released SP is important in the peripheral mechanism of NP. In the present study, the TRESK gene adenovirus vector significantly enhanced the TRESK mRNA and protein of the cultured rat DRG neurons. Radioimmunoassay analysis revealed that the capsaicin‑mediated SP release was significantly inhibited by the TRESK gene recombinant adenovirus vector in rat DRG neurons. These findings suggest that TRESK plays a role in adjusting the release of SP in DRG, which is related to NP.
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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.