ArticleProceedings of the National Academy of Sciences of the United States of America2011
Activity-dependent targeting of TRPV1 with a pore-permeating capsaicin analog.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- Article
- Toxigenic Clostridium perfringens Isolated from At-Risk Paediatric Inflammatory Bowel Disease Patients.Journal of Crohn's & colitis · 2024Article
- Blockade of TRPV channels by intracellular spermine.The Journal of general physiology · 2023Article
- Reply to "TRPA1-dependent calcium transients and CGRP release in DRG neurons require extracellular calcium".The Journal of cell biology · 2020Article
- Analgesic transient receptor potential vanilloid-1-active compounds inhibit native and recombinant T-type calcium channels.British journal of pharmacology · 2019Article
- Conformational plasticity in the selectivity filter of the TRPV2 ion channel.Nature structural & molecular biology · 2018Article
- Novobiocin, a Newly Found TRPV1 Inhibitor, Attenuates the Expression of TRPV1 in Rat Intestine and Intestinal Epithelial Cell Line IEC-6.Frontiers in pharmacology · 2018Article
- Plasmonic activation of gold nanorods for remote stimulation of calcium signaling and protein expression in HEK 293T cells.Biotechnology and bioengineering · 2016Article
- TRPV1 channel as a target for cancer therapy using CNT-based drug delivery systems.European biophysics journal : EBJ · 2016Article
- Principles and properties of ion flow in P2X receptors.Frontiers in cellular neuroscience · 2014Review
- Transient receptor potential channels as therapeutic targets.Nature reviews. Drug discovery · 2011Review
- Induction of TRPV1 desensitization by a biased receptor agonist.Channels (Austin, Tex.)Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The capsaicin receptor TRPV1 is the principal transduction channel for nociception. Excessive TRPV1 activation causes pathological pain. Ideal pain mangement requires selective inhibition of hyperactive pain-sensing neurons, but sparing normal nociception. We sought to determine whether it is possible to use activity-dependent TRPV1 agonists to identify nerves with excessive TRPV1 activity, as well as exploit the TRPV1 pore to deliver charged anesthetics for neuronal silencing. We synthesized a series of permanently charged capsaicinoids and found that one, cap-ET, efficaciously evoked TRPV1-dependent entry of Ca(2+) or the large cationic dye YO-PRO-1 comparably to capsaicin, but far smaller electrical currents. Cap-ET-induced YO-PRO-1 transport required permeation of both the agonist and the dye through the TRPV1 pore and could be enhanced by kinase activation or oxidative covalent modification. Moreover, cap-ET reduced capsaicin-induced currents by a voltage-dependent block of the pore. A low dose of cap-ET elicited entry of permanently charged Na(+) channel blockers to effectively suppress Na(+) currents in sensory neurons presensitized with oxidative chemicals. These results implicate therapeutic potential of these unique TRPV1 agonists exhibiting activity-dependent ion transport but of minimal pain-producing risks.
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