Evidence map›Paper›PMID 30888607›Full record

ArticleNeuroscience bulletin2019

Rac1 Modulates Excitatory Synaptic Transmission in Mouse Retinal Ganglion Cells.

Ling-Zhu Li, Ning Yin, Xue-Yan Li, Yanying Miao, Shuo Cheng, Fang Li, Guo-Li Zhao, Shu-Min Zhong, Xin Wang, Xiong-Li Yang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Neuroscience bulletin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 32% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
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  4. Sculpting Dendritic Spines during Initiation and Maintenance of Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Review
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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

11 authors at 3 institutions in 1 country.

Ling-Zhu LiDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Ning YinDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Xue-Yan LiDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Yanying MiaoDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Shuo ChengDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Fang LiDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Guo-Li ZhaoDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Shu-Min ZhongDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Xin WangDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Xiong-Li YangDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Zhongfeng WangDepartment of Neurology, Institutes of Brain Science, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. zfwang@fudan.edu.cn.
Zhongshan Hospital · CNFudan University · CNState Key Laboratory of Medical Neurobiology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ras-related C3 botulinum toxin substrate 1 (Rac1), a member of the Rho GTPase family which plays important roles in dendritic spine morphology and plasticity, is a key regulator of cytoskeletal reorganization in dendrites and spines. Here, we investigated whether and how Rac1 modulates synaptic transmission in mouse retinal ganglion cells (RGCs) using selective conditional knockout of Rac1 (Rac1-cKO). Rac1-cKO significantly reduced the frequency of AMPA receptor-mediated miniature excitatory postsynaptic currents, while glycine/GABA

Indexed as

AnimalsDendritesDendritic SpinesExcitatory Postsynaptic PotentialsGABA-A Receptor AntagonistsMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNeuropeptidesrac1 GTP-Binding ProteinReceptors, AMPAReceptors, GABA-AReceptors, GlycineReceptors, N-Methyl-D-AspartateRetinal Ganglion CellsGABA-A Receptor AntagonistsGprin1 protein, mouseNerve Tissue ProteinsNeuropeptidesNR2B NMDA receptorrac1 GTP-Binding ProteinRac1 protein, mouseReceptors, AMPAReceptors, GABA-AReceptors, GlycineReceptors, N-Methyl-D-AspartateDendriteDendritic spineExcitatory synaptic transmissionRac1Retinal ganglion cell

Identifiers

PMID30888607
PMCPMC6617495
OpenAlexW2939217272

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.