Evidence map›Paper›PMID 28899920›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

The TRPM1 Channel Is Required for Development of the Rod ON Bipolar Cell-AII Amacrine Cell Pathway in the Retinal Circuit.

Takashi Kozuka, Taro Chaya, Fuminobu Tamalu, Mariko Shimada, Kayo Fujimaki-Aoba, Ryusuke Kuwahara, Shu-Ichi Watanabe, Takahisa Furukawa

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 29% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Association Analysis Between Common Variants of theGenetic testing and molecular biomarkers · 2020
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. The Healthy and Diseased Retina Seen through Neuron-Glia Interactions.International journal of molecular sciences · 2024
    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

8 authors at 3 institutions in 1 country.

Takashi KozukaLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University.
Taro ChayaLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University.
Fuminobu TamaluDepartment of Physiology, Faculty of Medicine, Saitama Medical University, Saitama 350-0495, Japan, and.ORCID 0000-0002-2756-8822
Mariko ShimadaLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University.
Kayo Fujimaki-AobaDepartment of Physiology, Faculty of Medicine, Saitama Medical University, Saitama 350-0495, Japan, and.ORCID 0000-0003-2218-0009
Ryusuke KuwaharaResearch Center for Ultrahigh Voltage Electron Microscopy, Osaka University, Ibaraki, Osaka 567-0047, Japan.ORCID 0000-0002-7041-0828
Shu-Ichi WatanabeDepartment of Physiology, Faculty of Medicine, Saitama Medical University, Saitama 350-0495, Japan, and.
Takahisa FurukawaLaboratory for Molecular and Developmental Biology, Institute for Protein Research, Osaka University, takahisa.furukawa@protein.osaka-u.ac.jp.ORCID 0000-0003-4171-220X
Japan Science and Technology Agency · JPSaitama Medical University · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurotransmission plays an essential role in neural circuit formation in the central nervous system (CNS). Although neurotransmission has been recently clarified as a key modulator of retinal circuit development, the roles of individual synaptic transmissions are not yet fully understood. In the current study, we investigated the role of neurotransmission from photoreceptor cells to ON bipolar cells in development using mutant mouse lines of both sexes in which this transmission is abrogated. We found that deletion of the ON bipolar cation channel TRPM1 results in the abnormal contraction of rod bipolar terminals and a decreased number of their synaptic connections with amacrine cells. In contrast, these histological alterations were not caused by a disruption of total glutamate transmission due to loss of the ON bipolar glutamate receptor mGluR6 or the photoreceptor glutamate transporter VGluT1. In addition,

Indexed as

Amacrine CellsAnimalsChannelrhodopsinsDendritesFemaleGlutamic AcidIn Vitro TechniquesMaleMiceMice, KnockoutPatch-Clamp TechniquesRetinaRetinal Bipolar CellsRetinal Rod Photoreceptor CellsSynaptic TransmissionTRPM Cation ChannelsChannelrhodopsinsGlutamic AcidSlc17a7 protein, mouseTrpm1 protein, mouseTRPM Cation ChannelsVesicular Glutamate Transport Protein 1cation channelneurotransmissionretinaretinal circuit formation

Identifiers

PMID28899920
PMCPMC6596597
OpenAlexW2755173869

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.