Evidence map›Paper›PMID 34920740›Full record

ArticleJournal of neuroinflammation2021

Mechanisms underlying antidepressant effect of transcutaneous auricular vagus nerve stimulation on CUMS model rats based on hippocampal α7nAchR/NF-κB signal pathway.

Jun-Ying Wang, Yue Zhang, Yu Chen, Yu Wang, Shao-Yuan Li, Yi-Fei Wang, Zi-Xuan Zhang, Jinling Zhang, Peijing Rong

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 73 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 4 pooled it
4.8field-weighted citation impact, top 3% 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

73 citing papers in PubMed, 4 syntheses or guidelines pooled it, 128 citations in OpenAlex.

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13 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

9 authors at 1 institution in 1 country.

Jun-Ying Wang *Department of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Dongcheng District, No.16 Dongzhimen Nan Xiao Street, Beijing, 100700, China.
Yue Zhang *Department of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Dongcheng District, No.16 Dongzhimen Nan Xiao Street, Beijing, 100700, China.
Yu Chen *Department of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Dongcheng District, No.16 Dongzhimen Nan Xiao Street, Beijing, 100700, China.
Yu WangDepartment of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Dongcheng District, No.16 Dongzhimen Nan Xiao Street, Beijing, 100700, China.
Shao-Yuan LiDepartment of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Dongcheng District, No.16 Dongzhimen Nan Xiao Street, Beijing, 100700, China.
Yi-Fei WangDepartment of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Dongcheng District, No.16 Dongzhimen Nan Xiao Street, Beijing, 100700, China.
Zi-Xuan ZhangDepartment of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Dongcheng District, No.16 Dongzhimen Nan Xiao Street, Beijing, 100700, China.
Jinling ZhangDepartment of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Dongcheng District, No.16 Dongzhimen Nan Xiao Street, Beijing, 100700, China.
Peijing RongDepartment of Physiology, Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Dongcheng District, No.16 Dongzhimen Nan Xiao Street, Beijing, 100700, China. drrongpj@163.com.ORCID http://orcid.org/0000-0002-7288-2319
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

the Fundamental Research Funds for the Central Public Welfare Research Institutes ZZ13-YQ-062the Fundamental Research Funds for the Central Public Welfare Research Institutes ZZ201814002the Fundamental Research Funds for the Central Public Welfare Research Institutes ZZ20191603the National Key R&D Program of China 2018YFC1705803the Science and Technology Innovation Project of China Academy of Chinese Medical Sciences CI2021A03405
6 · The paper itself

Abstract

backgroundStress-induced neuroinflammation was considered to play a critical role in the pathogenesis of depression. Transcutaneous auricular vagus nerve stimulation (taVNS) is a relatively non-invasive alternative treatment for patients suffering from major depressive disorder. The anti-inflammatory signal of vagus nerve is mediated by α7 nicotinic acetylcholine receptor (α7nAchR), and the hippocampus, the region with the most distribution of α7nAchR, regulates emotions. Here, we investigated the role of α7nAchR mediating hippocampal neuroinflammation in taVNS antidepressant effect though homozygous α7nAChR (-/-) gene knockout and α7nAchR antagonist (methyllycaconitine, MLA).

methodsThere were control, model, taVNS, α7nAChR(-/-) + taVNS, hippocampus (Hi) MLA + taVNS and Hi saline + taVNS groups. We used the chronic unpredicted mild stress (CUMS) method to establish depressive model rats for 42 days, excepting control group. After the successful modeling, except the control and model, the rats in the other groups were given taVNS, which was applied through an electroacupuncture apparatus at the auricular concha (2/15 Hz, 2 mA, 30 min/days) for 21 days. Behavioral tests were conducted at baseline, after modeling and after taVNS intervention, including sucrose preference test (SPT), open field test (OFT) and forced swimming test (FST). These tests are widely used to evaluate depression-like behavior in rats. The samples were taken after experiment, the expressions of α7nAchR, NF-κB p65, IL-1β and the morphology of microglia were detected.

resultsDepression-like behavior and hippocampal neuroinflammation in CUMS model rats were manifested by down-regulated expression of α7nAchR, up-regulated expression of NF-κB p65 and IL-1β, and the morphology of microglia was in amoebic-like activated state. TaVNS could significantly reverse the above-mentioned phenomena, but had rare improvement effect for α7nAChR(-/-) rats and Hi MLA rats.

conclusionThe antidepressant effect of taVNS is related to hippocampal α7nAchR/NF-κB signal pathway.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsChronic DiseaseGene Knockout TechniquesHippocampusMajor Depressive DisorderMaleNicotinic AntagonistsRatsRats, Sprague-DawleyRats, TransgenicStress, PsychologicalTranscription Factor RelAVagus Nerve Stimulationalpha7 Nicotinic Acetylcholine ReceptorNicotinic AntagonistsTranscription Factor RelAAlpha 7 nicotinic acetylcholine receptorCytokinesDepressionNeuroinflammationTranscutaneous auricular vagus nerve stimulation

Identifiers

PMID34920740
PMCPMC8680337
OpenAlexW4200409452

What OpenQuestion holds

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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.