Evidence map›Paper›PMID 23713957›Full record

ArticleBritish journal of pharmacology2013

Spinal actions of ω-conotoxins, CVID, MVIIA and related peptides in a rat neuropathic pain model.

A Jayamanne, H J Jeong, C I Schroeder, R J Lewis, M J Christie, C W Vaughan

Open access · greenAbstract readComparative Study
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Peripheral CaeNeuro · 2024
    Article
  3. Peripheral CabioRxiv : the preprint server for biology · 2024
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  4. Interleukin-1α links peripheral CaScientific reports · 2024
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  5. Interleukin-1α links peripheral CabioRxiv : the preprint server for biology · 2024
    Article
  6. Article
  7. Heat But Not Mechanical Hypersensitivity Depends on Voltage-Gated CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  8. Article
  9. Article
  10. Article
  11. Spinal Fbxo3-Dependent Fbxl2 Ubiquitination of Active Zone Protein RIM1α Mediates Neuropathic Allodynia through CaV2.2 Activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  12. Article
  13. Molecular Targets of Cannabidiol in Neurological Disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

A JayamannePain Management Research Institute, Kolling Institute, Northern Clinical School, The University of Sydney, Sydney, NSW, Australia.
H J Jeong
C I Schroeder
R J Lewis
M J Christie
C W Vaughan
University of Sydney · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAntagonists of the N-type voltage gated calcium channel (VGCC), Cav 2.2, have a potentially important role in the treatment of chronic neuropathic pain. ω-conotoxins, such MVIIA and CVID are effective in neuropathic pain models. CVID is reported to have a greater therapeutic index than MVIIA in neuropathic pain models, and it has been suggested that this is due to faster reversibility of binding, but it is not known whether this can be improved further. EXPERIMENTAL APPROACH: We examined the potency of CVID, MVIIA and two intermediate hybrids ([K10R]CVID and [R10K]MVIIA) to reverse signs of neuropathic pain in a rat nerve ligation model in parallel with production of side effects. We also examined the potency and reversibility to inhibit primary afferent synaptic neurotransmission in rat spinal cord slices. KEY

resultsAll ω-conotoxins produced dose-dependent reduction in mechanical allodynia. They also produced side effects on the rotarod test and in a visual side-effect score. CVID displayed a marginally better therapeutic index than MVIIA. The hybrids had a lesser effect in the rotarod test than either of their parent peptides. Finally, the conotoxins all presynaptically inhibited excitatory synaptic neurotransmission into the dorsal horn and displayed recovery that was largely dependent upon the magnitude of inhibition and not the conotoxin type. CONCLUSIONS AND IMPLICATIONS: These findings indicate that CVID provides only a marginal improvement over MVIIA in a preclinical model of neuropathic pain, which appears to be unrelated to reversibility from binding. Hybrids of these conotoxins might provide viable alternative treatments.

Indexed as

Analgesics, Non-NarcoticAnimalsCalcium Channel BlockersDisease Models, AnimalDose-Response Relationship, DrugHyperalgesiaMaleNeuralgiaomega-ConotoxinsPeptidesRatsRats, Sprague-DawleyRotarod Performance TestSpinal CordSynaptic TransmissionAM336Analgesics, Non-NarcoticCalcium Channel Blockersomega-ConotoxinsPeptidesziconotidecalcium channelconotoxinneuropathicpainsynaptic neurotransmission

Identifiers

PMID23713957
PMCPMC3834750
OpenAlexW2133430337

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.