Evidence map›Paper›PMID 28708760›Full record

ArticlePain2017

Reactive oxygen species affect spinal cell type-specific synaptic plasticity in a model of neuropathic pain.

Alice Bittar, Jaebeom Jun, Jun-Ho La, Jigong Wang, Joong Woo Leem, Jin Mo Chung

Open access · greenAbstract read
In one paragraph

Article in Pain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.

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  14. Involvement of ROS signal in aging and regulation of brain functions.The journal of physiological sciences : JPS · 2025
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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

6 authors at 2 institutions in 2 countries.

Alice BittarDepartment of Neuroscience & Cell Biology, University of Texas Medical Branch, Galveston TX, USA.
Jaebeom JunDepartment of Neuroscience & Cell Biology, University of Texas Medical Branch, Galveston TX, USA.
Jun-Ho LaDepartment of Neuroscience & Cell Biology, University of Texas Medical Branch, Galveston TX, USA.
Jigong WangDepartment of Neuroscience & Cell Biology, University of Texas Medical Branch, Galveston TX, USA.
Joong Woo LeemDepartment of Physiology, Yonsei University College of Medicine, Seoul, South Korea.
Jin Mo ChungDepartment of Neuroscience & Cell Biology, University of Texas Medical Branch, Galveston TX, USA.
The University of Texas Medical Branch at Galveston · USYonsei University · KR

Funding

Mechanisms of Neuropathic PainR01NS031680 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI CHUNG, JIN M · 1994 to 2016
$4.1M
NINDS NIH HHS R01 NS031680
6 · The paper itself

Abstract

Spinal synaptic plasticity is believed to drive central sensitization that underlies the persistent nature of neuropathic pain. Our recent data showed that synaptic plasticity in the dorsal horn is cell type specific: intense afferent stimulation produced long-term potentiation (LTP) in excitatory spinothalamic tract neurons (STTn), whereas it produced long-term depression (LTD) in inhibitory GABAergic interneurons (GABAn). In addition, reactive oxygen species (ROS) were shown to be involved in LTP in STTn (STTn-LTP) and in LTD in GABAn (GABAn-LTD). This study examined the roles of 2 biologically important ROS--superoxide [·O2] and hydroxyl radicals [·OH]--in neuropathic mechanical hyperalgesia and cell type-specific spinal synaptic plasticity. The [·O2] donor induced stronger mechanical hyperalgesia than the [·OH] donor in naive mice. The [·O2] scavenger showed greater antihyperalgesic effect than [·OH] scavengers in the spinal nerve ligation (SNL) mouse model of neuropathic pain. In addition, the [·O2] donor induced both STTn-LTP and GABAn-LTD, but the [·OH] donor induced only GABAn-LTD. On the other hand, the [·O2] scavenger inhibited STTn-LTP and GABAn-LTD induction in naive mice and alleviated SNL-induced potentiation in STTn and depression in GABAn. The [·OH] scavenger, however, inhibited depression in GABAn but did not interfere with potentiation in STTn. These results indicate that mechanical hyperalgesia in SNL mice is the result of the combination of STTn-LTP and GABAn-LTD. Behavioral outcomes compliment electrophysiological results which suggest that [·O2] mediates both STTn-LTP and GABAn-LTD, whereas [·OH] is involved primarily in GABAn-LTD.

Indexed as

Afferent PathwaysAnimalsCyclic N-OxidesDisease Models, AnimalFree Radical ScavengersGABA AgentsGABAergic NeuronsGlutamate DecarboxylaseHydroxyl RadicalHyperalgesiaMaleMiceMice, Inbred C57BLMice, TransgenicNeuralgiaNeuronal Plasticity1,3-dimethylthioureaCyclic N-OxidesFree Radical ScavengersGABA AgentsGlutamate Decarboxylaseglutamate decarboxylase 1Hydroxyl RadicalReactive Oxygen SpeciesSpin LabelsSuperoxidestempolThiourea

Identifiers

PMID28708760
PMCPMC5963270
OpenAlexW2736305329

What OpenQuestion holds

Textmetadata
LicenceTDM
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.