Evidence map›Paper›PMID 29394316›Full record

ArticleBrain : a journal of neurology2018

Brain-derived neurotrophic factor derived from sensory neurons plays a critical role in chronic pain.

Shafaq Sikandar, Michael S Minett, Queensta Millet, Sonia Santana-Varela, Joanne Lau, John N Wood, Jing Zhao

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain : a journal of neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
10.7field-weighted citation impact, top 1% 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

107 citing papers in PubMed, 169 citations in OpenAlex.

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47 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Shafaq SikandarMolecular Nociception Group, Wolfson Institute for Biomedical Research, Division of Medicine, University College London, Gower Street London WC1E 6BT, UK.
Michael S MinettMolecular Nociception Group, Wolfson Institute for Biomedical Research, Division of Medicine, University College London, Gower Street London WC1E 6BT, UK.
Queensta MilletMolecular Nociception Group, Wolfson Institute for Biomedical Research, Division of Medicine, University College London, Gower Street London WC1E 6BT, UK.
Sonia Santana-VarelaMolecular Nociception Group, Wolfson Institute for Biomedical Research, Division of Medicine, University College London, Gower Street London WC1E 6BT, UK.
Joanne LauMolecular Nociception Group, Wolfson Institute for Biomedical Research, Division of Medicine, University College London, Gower Street London WC1E 6BT, UK.
John N WoodMolecular Nociception Group, Wolfson Institute for Biomedical Research, Division of Medicine, University College London, Gower Street London WC1E 6BT, UK.
Jing ZhaoMolecular Nociception Group, Wolfson Institute for Biomedical Research, Division of Medicine, University College London, Gower Street London WC1E 6BT, UK.
University College London · GB

Funding

Arthritis Research UK 507928Medical Research Council G091905Wellcome Trust 101054/Z/13/ZWellcome Trust 200183/Z/15/Z
6 · The paper itself

Abstract

Many studies support the pro-nociceptive role of brain-derived neurotrophin factor (BDNF) in pain processes in the peripheral and central nervous system. We have previously shown that nociceptor-derived BDNF is involved in inflammatory pain. Microglial-derived BDNF has also been shown to be involved in neuropathic pain. However, the distinct contribution of primary afferent-derived BNDF to chronic pain processing remains undetermined. In this study, we used Avil-CreERT2 mice to delete Bdnf from all adult peripheral sensory neurons. Conditional BDNF knockouts were healthy with no sensory neuron loss. Behavioural assays and in vivo electrophysiology indicated that spinal excitability was normal. Following formalin inflammation or neuropathy with a modified Chung model, we observed normal development of acute pain behaviour, but a deficit in second phase formalin-induced nocifensive responses and a reversal of neuropathy-induced mechanical hypersensitivity during the later chronic pain phase in conditional BDNF knockout mice. In contrast, we observed normal development of acute and chronic neuropathic pain in the Seltzer model, indicating differences in the contribution of BDNF to distinct models of neuropathy. We further used a model of hyperalgesic priming to examine the contribution of primary afferent-derived BDNF in the transition from acute to chronic pain, and found that primed BDNF knockout mice do not develop prolonged mechanical hypersensitivity to an inflammatory insult. Our data suggest that BDNF derived from sensory neurons plays a critical role in mediating the transition from acute to chronic pain.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCarrageenanChronic PainDisease Models, AnimalFemaleFormaldehydeGanglia, SpinalHyperalgesiaMaleMiceMice, TransgenicMicrofilament ProteinsPain MeasurementSensory Receptor CellsAvil protein, mouseBrain-Derived Neurotrophic FactorCarrageenanFormaldehydeMicrofilament Proteins

Identifiers

PMID29394316
PMCPMC5888992
OpenAlexW2776476861

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.