Evidence map›Paper›PMID 33854034›Full record

ArticleCell death & disease2021

Spine impairment in mice high-expressing neuregulin 1 due to LIMK1 activation.

Peng Chen, Hongyang Jing, Mingtao Xiong, Qian Zhang, Dong Lin, Dongyan Ren, Shunqi Wang, Dongmin Yin, Yongjun Chen, Tian Zhou and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. 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
3.8field-weighted citation impact, top 5% 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, 41 citations in OpenAlex.

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  14. DSCAM Deficiency Leads to Premature Spine Maturation and Autism-like Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
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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 3 institutions in 1 country.

Peng Chen *School of Life Sciences, Nanchang University, Nanchang, 330031, China.
Hongyang Jing *School of Life Sciences, Nanchang University, Nanchang, 330031, China.
Mingtao XiongInstitute of Life Science, Nanchang University, Nanchang, 330031, China.
Qian ZhangSchool of Basic Medical Sciences, Nanchang University, Nanchang, 330031, China.
Dong LinSchool of Life Sciences, Nanchang University, Nanchang, 330031, China.
Dongyan RenSchool of Life Sciences, Nanchang University, Nanchang, 330031, China.
Shunqi WangSchool of Life Sciences, Nanchang University, Nanchang, 330031, China.
Dongmin YinKey Laboratory of Brain Functional Genomics, Ministry of Education and Shanghai, School of Life Science, East China Normal University, Shanghai, 200062, China.ORCID 0000-0001-9329-050X
Yongjun ChenSouth China Research Center for Acupuncture and Moxibustion, Medical College of Acu-Moxi and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Tian ZhouSchool of Basic Medical Sciences, Nanchang University, Nanchang, 330031, China.
Baoming LiInstitute of Life Science, Nanchang University, Nanchang, 330031, China.
Erkang FeiSchool of Life Sciences, Nanchang University, Nanchang, 330031, China. fek@ncu.edu.cn.
Bing-Xing PanSchool of Life Sciences, Nanchang University, Nanchang, 330031, China. panbingxing@ncu.edu.cn.
Nanchang University · CNEast China Normal University · CNGuangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The genes encoding for neuregulin1 (NRG1), a growth factor, and its receptor ErbB4 are both risk factors of major depression disorder and schizophrenia (SZ). They have been implicated in neural development and synaptic plasticity. However, exactly how NRG1 variations lead to SZ remains unclear. Indeed, NRG1 levels are increased in postmortem brain tissues of patients with brain disorders. Here, we studied the effects of high-level NRG1 on dendritic spine development and function. We showed that spine density in the prefrontal cortex and hippocampus was reduced in mice (ctoNrg1) that overexpressed NRG1 in neurons. The frequency of miniature excitatory postsynaptic currents (mEPSCs) was reduced in both brain regions of ctoNrg1 mice. High expression of NRG1 activated LIMK1 and increased cofilin phosphorylation in postsynaptic densities. Spine reduction was attenuated by inhibiting LIMK1 or blocking the NRG1-LIMK1 interaction, or by restoring NRG1 protein level. These results indicate that a normal NRG1 protein level is necessary for spine homeostasis and suggest a pathophysiological mechanism of abnormal spines in relevant brain disorders.

Indexed as

AnimalsExcitatory Postsynaptic PotentialsHippocampusLim KinasesMiceNeuregulin-1Neuronal PlasticityNeuronsReceptor, ErbB-4SpineSynapsesLimk1 protein, mouseLim KinasesNeuregulin-1Nrg1 protein, mouseReceptor, ErbB-4

Identifiers

PMID33854034
PMCPMC8047019
OpenAlexW3155943403

What Socratic holds

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LicenceCC BY
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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 Socratic graph.