ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Reducing agents sensitize C-type nociceptors by relieving high-affinity zinc inhibition of T-type calcium channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
59 citing papers in PubMed, 149 citations in OpenAlex.
- T-type calcium channel modulation by hydrogen sulfide in neuropathic pain conditions.Frontiers in pharmacology · 2023Review
- The Tarantula Toxin ω-Avsp1a Specifically Inhibits Human CaBiomedicines · 2022Article
- L-cysteine modulates visceral nociception mediated by the CaPflugers Archiv : European journal of physiology · 2022Article
- The Mechanisms of Plasticity of Nociceptive Ion Channels in Painful Diabetic Neuropathy.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- Targeting T-type/CaV3.2 channels for chronic pain.Translational research : the journal of laboratory and clinical medicine · 2021Review
- Neuromedin B receptor stimulation of Cav3.2 T-type CaTheranostics · 2021Article
- Endothelial Nitric Oxide Suppresses Action-Potential-Like Transient Spikes and Vasospasm in Small Resistance Arteries.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Unique cysteine-enriched, D2L5 and D4L6 extracellular loops in CaScientific reports · 2020Article
- Delineating an extracellular redox-sensitive module in T-type CaThe Journal of biological chemistry · 2020Article
- Glycosylation of CaFrontiers in cellular neuroscience · 2020Article
- Pathophysiological roles and therapeutic potential of voltage-gated ion channels (VGICs) in pain associated with herpesvirus infection.Cell & bioscience · 2020Review
- Reductive Reprogramming: A Not-So-Radical Hypothesis of Neurodegeneration Linking Redox Perturbations to Neuroinflammation and Excitotoxicity.Cellular and molecular neurobiology · 2019Review
- Cholecystokinin type B receptor-mediated inhibition of A-type KCell communication and signaling : CCS · 2019Article
- Selective inhibition of CaScience signaling · 2018Article
- Chemical Biology of HChemical reviews · 2018Review
- Modulatory features of the novel spider toxin μ-TRTX-Df1a isolated from the venom of the spider Davus fasciatus.British journal of pharmacology · 2017Article
- Redox-Dependent Modulation of T-Type Ca(2+) Channels in Sensory Neurons Contributes to Acute Anti-Nociceptive Effect of Substance P.Antioxidants & redox signaling · 2016Article
- Regulation of the T-type Ca(2+) channel Cav3.2 by hydrogen sulfide: emerging controversies concerning the role of H2 S in nociception.The Journal of physiology · 2016Review
- Genetic alteration of the metal/redox modulation of Cav3.2 T-type calcium channel reveals its role in neuronal excitability.The Journal of physiology · 2016Article
- Painful Diabetic Neuropathy: Prevention or Suppression?International review of neurobiology · 2016Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Recent studies have demonstrated an important role for T-type Ca2+ channels (T-channels) in controlling the excitability of peripheral pain-sensing neurons (nociceptors). However, the molecular mechanisms underlying the functions of T-channels in nociceptors are poorly understood. Here, we demonstrate that reducing agents as well as endogenous metal chelators sensitize C-type dorsal root ganglion nociceptors by chelating Zn2+ ions off specific extracellular histidine residues on Ca(v)3.2 T-channels, thus relieving tonic channel inhibition, enhancing Ca(v)3.2 currents, and lowering the threshold for nociceptor excitability in vitro and in vivo. Collectively, these findings describe a novel mechanism of nociceptor sensitization and firmly establish reducing agents, as well as Zn2+, Zn2+-chelating amino acids, and Zn2+-chelating proteins as endogenous modulators of Ca(v)3.2 and nociceptor excitability.
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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.