Evidence map›Paper›PMID 34544832›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2021

Studying Independent

Liam J Peck, Ryan Patel, Paula Diaz, Yolanda M Wintle, Anthony H Dickenson, Andrew J Todd, Margarita Calvo, David L H Bennett

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Liam J PeckNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, United Kingdom liam.peck@sjc.ox.ac.uk david.bennett@ndcn.ox.ac.uk.ORCID 0000-0001-9501-1762
Ryan PatelDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, WC1E 6BT, United Kingdom.
Paula DiazDepartamento de Fisiologia, Facultad de Ciencias Biologicas, Pontificia Universidad Catolica de Chile and Millennium Nucleus for the Study of Pain, Santiago, 8330025, Chile.
Yolanda M WintleNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, United Kingdom.
Anthony H DickensonDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, WC1E 6BT, United Kingdom.
Andrew J ToddInstitute of Neuroscience and Psychology, University of Glasgow, Glasgow, G12 8QQ, United Kingdom.ORCID 0000-0002-3007-6749
Margarita CalvoDepartamento de Fisiologia, Facultad de Ciencias Biologicas, Pontificia Universidad Catolica de Chile and Millennium Nucleus for the Study of Pain, Santiago, 8330025, Chile.
David L H BennettNuffield Department of Clinical Neurosciences, University of Oxford, Oxford, OX3 9DU, United Kingdom liam.peck@sjc.ox.ac.uk david.bennett@ndcn.ox.ac.uk.ORCID 0000-0002-7996-2696
University of Oxford · GBPontificia Universidad Católica de Chile · CLUniversity College London · GBUniversity of Glasgow · GB

Funding

Wellcome Trust 102645Wellcome Trust 109117Wellcome Trust 202747Wellcome Trust 219433
6 · The paper itself

Abstract

The potassium channel Kv1.6 has recently been implicated as a major modulatory channel subunit expressed in primary nociceptors. Furthermore, its expression at juxtaparanodes of myelinated primary afferents is induced following traumatic nerve injury as part of an endogenous mechanism to reduce hyperexcitability and pain-related hypersensitivity. In this study, we compared two mouse models of constitutive Kv1.6 knock-out (KO) achieved by different methods: traditional gene trap via homologous recombination and CRISPR-mediated excision. Both Kv1.6 KO mouse lines exhibited an unexpected reduction in sensitivity to noxious heat stimuli, to differing extents: the Kv1.6 mice produced via gene trap had a far more significant hyposensitivity. These mice (

Indexed as

Genes, ReporterLac OperonAnimalsCRISPR-Cas SystemsFemaleGene Knockout TechniquesIntegrasesKv1.6 Potassium ChannelMaleMiceMice, Inbred C57BLNeuralgiaNociceptorsSynapsesCre recombinaseIntegrasesKcna6 protein, mouseKv1.6 Potassium ChannelgangliosidesKv1.6LacZneuropathic painnociceptionpain

Identifiers

PMID34544832
PMCPMC8570829
OpenAlexW3200584304

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.