Evidence map›Paper›PMID 25354791›Full record

ArticleNature communications2014

Presynaptic GABAergic inhibition regulated by BDNF contributes to neuropathic pain induction.

Jeremy Tsung-chieh Chen, Da Guo, Dario Campanelli, Flavia Frattini, Florian Mayer, Luming Zhou, Rohini Kuner, Paul A Heppenstall, Marlies Knipper, Jing Hu

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

43 citing papers in PubMed, 102 citations in OpenAlex.

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  13. Pre-Synaptic GABACells · 2022
    Article
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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

10 authors at 4 institutions in 2 countries.

Jeremy Tsung-chieh ChenCentre for Integrative Neuroscience, Otfried-Mueller-Strasse 25, 72076 Tübingen, Germany.
Da GuoCentre for Integrative Neuroscience, Otfried-Mueller-Strasse 25, 72076 Tübingen, Germany.
Dario Campanelli1] Centre for Integrative Neuroscience, Otfried-Mueller-Strasse 25, 72076 Tübingen, Germany [2] Hearing Research Centre, Elfriede Aulhornstrasse 5, 72076 Tübingen, Germany.
Flavia FrattiniCentre for Integrative Neuroscience, Otfried-Mueller-Strasse 25, 72076 Tübingen, Germany.
Florian MayerCentre for Integrative Neuroscience, Otfried-Mueller-Strasse 25, 72076 Tübingen, Germany.
Luming ZhouLaboratory for NeuroRegeneration and Repair, Center for Neurology, Hertie Institute for Clinical Brain Research, 72076 Tübingen, Germany.
Rohini KunerPharmacology Institute, University of Heidelberg, Im Neuenheimer Feld 584, 69120 Heidelberg, Germany.
Paul A HeppenstallMouse Biology Unit, European Molecular Biology Laboratory (EMBL), Via Ramarini 32, 00016 Monterotondo, Italy.
Marlies KnipperHearing Research Centre, Elfriede Aulhornstrasse 5, 72076 Tübingen, Germany.
Jing HuCentre for Integrative Neuroscience, Otfried-Mueller-Strasse 25, 72076 Tübingen, Germany.
Bernstein Center for Computational Neuroscience Tübingen · DEEuropean Molecular Biology Laboratory · ITHeidelberg University · DEHertie Institute for Clinical Brain Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gate control theory proposes the importance of both pre- and post-synaptic inhibition in processing pain signal in the spinal cord. However, although postsynaptic disinhibition caused by brain-derived neurotrophic factor (BDNF) has been proved as a crucial mechanism underlying neuropathic pain, the function of presynaptic inhibition in acute and neuropathic pain remains elusive. Here we show that a transient shift in the reversal potential (EGABA) together with a decline in the conductance of presynaptic GABAA receptor result in a reduction of presynaptic inhibition after nerve injury. BDNF mimics, whereas blockade of BDNF signalling reverses, the alteration in GABAA receptor function and the neuropathic pain syndrome. Finally, genetic disruption of presynaptic inhibition leads to spontaneous development of behavioural hypersensitivity, which cannot be further sensitized by nerve lesions or BDNF. Our results reveal a novel effect of BDNF on presynaptic GABAergic inhibition after nerve injury and may represent new strategy for treating neuropathic pain.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorGanglia, SpinalMaleMiceMice, KnockoutNeuralgiaNociceptionNociceptorsPresynaptic TerminalsReceptors, GABA-ABrain-Derived Neurotrophic FactorReceptors, GABA-A

Identifiers

PMID25354791
PMCPMC4220496
OpenAlexW2037106314

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.