Evidence map›Paper›PMID 32051342›Full record

ArticleJCI insight2020

Microglial depletion under thalamic hemorrhage ameliorates mechanical allodynia and suppresses aberrant axonal sprouting.

Shin-Ichiro Hiraga, Takahide Itokazu, Maki Hoshiko, Hironobu Takaya, Mariko Nishibe, Toshihide Yamashita

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  9. Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024
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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 3 institutions in 2 countries.

Shin-Ichiro HiragaDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Takahide ItokazuDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Maki HoshikoDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Hironobu TakayaDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Mariko NishibeDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
Toshihide YamashitaDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan.
The University of Osaka · JPNeuro Pain Medical Center · USUbe Frontier University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Central poststroke pain (CPSP) is one of the neuropathic pain syndromes that can occur following stroke involving the somatosensory system. However, the underlying mechanism of CPSP remains largely unknown. Here, we established a CPSP mouse model by inducing a focal hemorrhage in the thalamic ventrobasal complex and confirmed the development of mechanical allodynia. In this model, microglial activation was observed in the somatosensory cortex, as well as in the injured thalamus. By using a CSF1 receptor inhibitor, we showed that microglial depletion effectively prevented allodynia development in our CPSP model. In the critical phase of allodynia development, c-fos-positive neurons increased in the somatosensory cortex, accompanied by ectopic axonal sprouting of the thalamocortical projection. Furthermore, microglial ablation attenuated both neuronal hyperactivity in the somatosensory cortex and circuit reorganization. These findings suggest that microglia play a crucial role in the development of CPSP pathophysiology by promoting sensory circuit reorganization.

Indexed as

AnimalsAxonsCerebral HemorrhageDisease Models, AnimalHyperalgesiaMiceMicrogliaNeuralgiaThalamusInflammationNeurosciencePain

Identifiers

PMID32051342
PMCPMC7098795
OpenAlexW3005912714

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.