Evidence map›Paper›PMID 30532543›Full record

ArticleNeuropsychiatric disease and treatment2018

Activation of ERK/CREB/BDNF pathway involved in abnormal behavior of neonatally Borna virus-infected rats.

Chenmeng Li, Xiaoyan Xu, Xiong Zhang, Ke Cheng, Yujie Guo, Jie Jie, Hua Guo, Yong He, Chanjuan Zhou, Siwen Gui and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuropsychiatric disease and treatment, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. 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

13 authors at 2 institutions in 1 country.

Chenmeng LiDepartment of Neurology, Yongchuan Hospital of Chongqing Medical University, Chongqing 402460, China, xiepeng@cqmu.edu.cn.
Xiaoyan XuDepartment of Neurology Institute of Neuroscience and Collaborative Innovation Center for Brain Science, Chongqing Medical University, Chongqing 400016, China, xiepeng@cqmu.edu.cn.
Xiong ZhangDepartment of Neurology Institute of Neuroscience and Collaborative Innovation Center for Brain Science, Chongqing Medical University, Chongqing 400016, China, xiepeng@cqmu.edu.cn.
Ke ChengDepartment of Neurology Institute of Neuroscience and Collaborative Innovation Center for Brain Science, Chongqing Medical University, Chongqing 400016, China, xiepeng@cqmu.edu.cn.
Yujie GuoDepartment of Neurology, Yongchuan Hospital of Chongqing Medical University, Chongqing 402460, China, xiepeng@cqmu.edu.cn.
Jie JieDepartment of Neurology, Yongchuan Hospital of Chongqing Medical University, Chongqing 402460, China, xiepeng@cqmu.edu.cn.
Hua GuoDepartment of Neurology, Yongchuan Hospital of Chongqing Medical University, Chongqing 402460, China, xiepeng@cqmu.edu.cn.
Yong HeDepartment of Neurology, Yongchuan Hospital of Chongqing Medical University, Chongqing 402460, China, xiepeng@cqmu.edu.cn.
Chanjuan ZhouDepartment of Neurology Institute of Neuroscience and Collaborative Innovation Center for Brain Science, Chongqing Medical University, Chongqing 400016, China, xiepeng@cqmu.edu.cn.
Siwen GuiDepartment of Neurology Institute of Neuroscience and Collaborative Innovation Center for Brain Science, Chongqing Medical University, Chongqing 400016, China, xiepeng@cqmu.edu.cn.
Xiaogang ZhongDepartment of Neurology Institute of Neuroscience and Collaborative Innovation Center for Brain Science, Chongqing Medical University, Chongqing 400016, China, xiepeng@cqmu.edu.cn.
Haiyang WangDepartment of Neurology Institute of Neuroscience and Collaborative Innovation Center for Brain Science, Chongqing Medical University, Chongqing 400016, China, xiepeng@cqmu.edu.cn.
Peng XieDepartment of Neurology, Yongchuan Hospital of Chongqing Medical University, Chongqing 402460, China, xiepeng@cqmu.edu.cn.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuropsychiatric disorders are devastating illnesses worldwide; however, the potential involvement of viruses in the pathophysiological mechanisms of psychiatric diseases have not been clearly elucidated. Borna disease virus (BDV) is a neurotropic, noncytopathic RNA virus. MATERIALS AND

methodsIn this study, we infected neonatal rats intracranially with BDV Hu-H1 and Strain V within 24 hours of birth. Psychological phenotypes were assessed using sucrose preference test, open field test, elevated plus maze test, and forced swim test. The protein expression of ERK/CREB/BDNF pathway was assessed by Western blotting of in vitro and in vivo samples.

resultsHu-H1-infected rats showed anxiety-like behavior 8 weeks postinfection while Strain V-infected rats demonstrated a certain abnormal behavior. Phosphorylated ERK1/2 was significantly upregulated in the hippocampi of Strain V- and Hu-H1-infected rats compared with control rats, indicating that Raf/MEK/ERK signaling was activated.

conclusionThe data suggested that infection of neonatal rats with BDV Hu-H1 and Strain V caused behavioral abnormalities that shared common molecular pathways, providing preliminary evidences to investigate the underlying mechanisms of psychiatric disorders caused by BDV.

Indexed as

Borna disease virusERK/CREB/BDNF signaling pathwayneonatal Borna disease

Identifiers

PMID30532543
PMCPMC6247968
OpenAlexW2901848408

What OpenQuestion holds

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LicenceCC BY-NC
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.