Evidence map›Paper›PMID 25995483›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Prdm13 regulates subtype specification of retinal amacrine interneurons and modulates visual sensitivity.

Satoshi Watanabe, Rikako Sanuki, Yuko Sugita, Wataru Imai, Ryoji Yamazaki, Takashi Kozuka, Mizuki Ohsuga, Takahisa Furukawa

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Article
  3. Nox3 expression and function in retinal ganglion cells and Amacrine cells.Cellular and molecular life sciences : CMLS · 2025
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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

8 authors at 3 institutions in 1 country.

Satoshi WatanabeLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University, JST, Core Research for Evolutional Science and Technology, 3-2 Yamadaoka, Suita, Osaka, 565-0871, Japan, and Kyoto University Graduate School of Medicine, Yoshida-konoe, Sakyo-ku, 606-8501, Kyoto, Japan.
Rikako SanukiLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University, JST, Core Research for Evolutional Science and Technology, 3-2 Yamadaoka, Suita, Osaka, 565-0871, Japan, and.
Yuko SugitaLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University, JST, Core Research for Evolutional Science and Technology, 3-2 Yamadaoka, Suita, Osaka, 565-0871, Japan, and.
Wataru ImaiLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University.
Ryoji YamazakiLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University, JST, Core Research for Evolutional Science and Technology, 3-2 Yamadaoka, Suita, Osaka, 565-0871, Japan, and.
Takashi KozukaLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University.
Mizuki OhsugaLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University.
Takahisa FurukawaLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University, JST, Core Research for Evolutional Science and Technology, 3-2 Yamadaoka, Suita, Osaka, 565-0871, Japan, and takahisa.furukawa@protein.osaka-u.ac.jp.ORCID http://orcid.org/0000-0003-4171-220X
The University of Osaka · JPKyoto University · JPProtein Research Foundation · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amacrine interneurons, which are highly diversified in morphological, neurochemical, and physiological features, play crucial roles in visual information processing in the retina. However, the specification mechanisms and functions in vision for each amacrine subtype are not well understood. We found that the Prdm13 transcriptional regulator is specifically expressed in developing and mature amacrine cells in the mouse retina. Most Prdm13-positive amacrine cells are Calbindin- and Calretinin-positive GABAergic or glycinergic neurons. Absence of Prdm13 significantly reduces GABAergic and glycinergic amacrines, resulting in a specific defect of the S2/S3 border neurite bundle in the inner plexiform layer. Forced expression of Prdm13 distinctively induces GABAergic and glycinergic amacrine cells but not cholinergic amacrine cells, whereas Ptf1a, an upstream transcriptional regulator of Prdm13, induces all of these subtypes. Moreover, Prdm13-deficient mice showed abnormally elevated spatial, temporal, and contrast sensitivities in vision. Together, these results show that Prdm13 regulates development of a subset of amacrine cells, which newly defines an amacrine subtype to negatively modulate visual sensitivities. Our current study provides new insights into mechanisms of the diversification of amacrine cells and their function in vision.

Indexed as

Contrast SensitivityAmacrine CellsAnimalsCholinergic NeuronsGABAergic NeuronsHistone-Lysine N-MethyltransferaseInterneuronsMiceNeurogenesisTranscription FactorsHistone-Lysine N-MethyltransferasePrdm13 protein, mouseTranscription Factorsamacrine cellinterneuronPrdm13retinasubtype specificationvisual function

Identifiers

PMID25995483
PMCPMC6795186
OpenAlexW1820330395

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.