Evidence map›Paper›PMID 33402212›Full record

ArticleJournal of neuroinflammation2021

Microglial deletion and inhibition alleviate behavior of post-traumatic stress disorder in mice.

Shuoshuo Li, Yajin Liao, Yuan Dong, Xiaoheng Li, Jun Li, Yong Cheng, Jinbo Cheng, Zengqiang Yuan

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Sex-specific role of microglia in ΔNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  19. The therapeutic effects ofGut microbiome (Cambridge, England) · 2025
    Review
  20. Review

1 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

8 authors at 4 institutions in 1 country.

Shuoshuo LiThe Brain Science Center, Beijing Institute of Basic Medical Sciences, No. 27 Taiping Road, Haidian District, Beijing, 100850, China.
Yajin LiaoCenter on Translational Neuroscience, College of Life & Environmental Science, Minzu University of China, Beijing, 100081, China.
Yuan DongDepartment of Biochemistry, Medical College, Qingdao University, Qingdao, 266071, Shandong, China.
Xiaoheng LiThe Brain Science Center, Beijing Institute of Basic Medical Sciences, No. 27 Taiping Road, Haidian District, Beijing, 100850, China.
Jun LiBeijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China.
Yong ChengCenter on Translational Neuroscience, College of Life & Environmental Science, Minzu University of China, Beijing, 100081, China.
Jinbo ChengCenter on Translational Neuroscience, College of Life & Environmental Science, Minzu University of China, Beijing, 100081, China. cheng_jinbo@126.com.
Zengqiang YuanThe Brain Science Center, Beijing Institute of Basic Medical Sciences, No. 27 Taiping Road, Haidian District, Beijing, 100850, China. zqyuan@bmi.ac.cn.ORCID http://orcid.org/0000-0001-5739-2867
Minzu University of China · CNCapital Medical University · CNChinese Institute for Brain Research · CNQingdao University · CN

Funding

National Natural Science Foundation of China 81701187National Natural Science Foundation of China 81870839National Natural Science Foundation of China 81930029 & 81630026
6 · The paper itself

Abstract

backgroundAlteration of immune status in the central nervous system (CNS) has been implicated in the development of post-traumatic stress disorder (PTSD). However, the nature of overall changes in brain immunocyte landscape in PTSD condition remains unclear.

methodsWe constructed a mouse PTSD model by electric foot-shocks followed by contextual reminders and verified the PTSD-related symptoms by behavior test (including contextual freezing test, open-field test, and elevated plus maze test). We examined the immunocyte panorama in the brains of the naïve or PTSD mice by using single-cell mass cytometry. Microglia number and morphological changes in the hippocampus, prefrontal cortex, and amygdala were analyzed by histopathological methods. The gene expression changes of those microglia were detected by quantitative real-time PCR. Genetic/pharmacological depletion of microglia or minocycline treatment before foot-shocks exposure was performed to study the role of microglia in PTSD development and progress.

resultsWe found microglia are the major brain immune cells that respond to PTSD. The number of microglia and ratio of microglia to immunocytes was significantly increased on the fifth day of foot-shock exposure. Furthermore, morphological analysis and gene expression profiling revealed temporal patterns of microglial activation in the hippocampus of the PTSD brains. Importantly, we found that genetic/pharmacological depletion of microglia or minocycline treatment before foot-shock exposure alleviated PTSD-associated anxiety and contextual fear.

conclusionOur results demonstrated a critical role for microglial activation in PTSD development and a potential therapeutic strategy for the clinical treatment of PTSD in the form of microglial inhibition.

Indexed as

AnimalsAnxietyElectric StimulationFearMaleMaze LearningMiceMice, TransgenicMicrogliaMinocyclineStress Disorders, Post-TraumaticStress, PsychologicalMinocyclineMass cytometryMicrogliaMicroglial activationMicroglial depletionPTSD

Identifiers

PMID33402212
PMCPMC7786489
OpenAlexW3120239382

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.