ArticleBritish journal of pharmacology2013
Pharmacological fractionation of tetrodotoxin-sensitive sodium currents in rat dorsal root ganglion neurons by μ-conotoxins.
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Functional role of Nav1.8 channels in action potentials of mouse CGRP-lineage dorsal root ganglion neurons.The Journal of physiology · 2026Article
- Marine-derived bioactive compounds for neuropathic pain: pharmacology and therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- DecipheringFrontiers in cellular neuroscience · 2021Article
- Mining the NaBiochemical pharmacology · 2019Review
- Gi-DREADD Expression in Peripheral Nerves Produces Ligand-Dependent Analgesia, as well as Ligand-Independent Functional Changes in Sensory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Roles of Voltage-Gated Tetrodotoxin-Sensitive Sodium Channels NaV1.3 and NaV1.7 in Diabetes and Painful Diabetic Neuropathy.International journal of molecular sciences · 2016Review
- Characterization of Endogenous Sodium Channels in the ND7-23 Neuroblastoma Cell Line: Implications for Use as a Heterologous Ion Channel Expression System Suitable for Automated Patch Clamp Screening.Assay and drug development technologies · 2016Article
- The hitchhiker's guide to the voltage-gated sodium channel galaxy.The Journal of general physiology · 2016Review
- EXPRESS: Voltage-dependent sodium (NaV) channels in group IV sensory afferents.Molecular pain · 2016Article
- Α- and β-subunit composition of voltage-gated sodium channels investigated with μ-conotoxins and the recently discovered μO§-conotoxin GVIIJ.Journal of neurophysiology · 2015Article
- Discovery by proteogenomics and characterization of an RF-amide neuropeptide from cone snail venom.Journal of proteomics · 2015Article
- Structure and function of μ-conotoxins, peptide-based sodium channel blockers with analgesic activity.Future medicinal chemistry · 2014Review
- A disulfide tether stabilizes the block of sodium channels by the conotoxin μO§-GVIIJ.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Animal toxins influence voltage-gated sodium channel function.Handbook of experimental pharmacology · 2014Review
- Article
- Designing a C84 fullerene as a specific voltage-gated sodium channel blocker.Nanoscale research letters · 2013Article
- Co-expression of Na(V)β subunits alters the kinetics of inhibition of voltage-gated sodium channels by pore-blocking μ-conotoxins.British journal of pharmacology · 2013Article
- Enhanced trafficking of an inherited erythromelalgia NaNeurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
background and purposeAdult rat dorsal root ganglion (DRG) neurons normally express transcripts for five isoforms of the α-subunit of voltage-gated sodium channels: NaV 1.1, 1.6, 1.7, 1.8 and 1.9. Tetrodotoxin (TTX) readily blocks all but NaV 1.8 and 1.9, and pharmacological agents that discriminate among the TTX-sensitive NaV 1-isoforms are scarce. Recently, we used the activity profile of a panel of μ-conotoxins in blocking cloned rodent NaV 1-isoforms expressed in Xenopus laevis oocytes to conclude that action potentials of A- and C-fibres in rat sciatic nerve were, respectively, mediated primarily by NaV 1.6 and NaV 1.7. EXPERIMENTAL APPROACH: We used three μ-conotoxins, μ-TIIIA, μ-PIIIA and μ-SmIIIA, applied individually and in combinations, to pharmacologically differentiate the TTX-sensitive INa of voltage-clamped neurons acutely dissociated from adult rat DRG. We examined only small and large neurons whose respective INa were >50% and >80% TTX-sensitive. KEY
resultsIn both small and large neurons, the ability of the toxins to block TTX-sensitive INa was μ-TIIIA < μ-PIIIA < μ-SmIIIA, with the latter blocking ≳90%. Comparison of the toxin-susceptibility profiles of the neuronal INa with recently acquired profiles of rat NaV 1-isoforms, co-expressed with various NaV β-subunits in X. laevis oocytes, were consistent: NaV 1.1, 1.6 and 1.7 could account for all of the TTX-sensitive INa , with NaV 1.1 < NaV 1.6 < NaV 1.7 for small neurons and NaV 1.7 < NaV 1.1 < NaV 1.6 for large neurons. CONCLUSIONS AND IMPLICATIONS: Combinations of μ-conotoxins can be used to determine the probable NaV 1-isoforms underlying the INa in DRG neurons. Preliminary experiments with sympathetic neurons suggest that this approach is extendable to other neurons.
Indexed as
Identifiers
What OpenQuestion holds
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.