Evidence map›Paper›PMID 29854741›Full record

ArticleBioMed research international2018

Different Activity Patterns in Retinal Ganglion Cells of TRPM1 and mGluR6 Knockout Mice.

Haruki Takeuchi, Sho Horie, Satoru Moritoh, Hiroki Matsushima, Tesshu Hori, Yoshitaka Kimori, Katsunori Kitano, Yasuhiro Tsubo, Masao Tachibana, Chieko Koike

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. The Healthy and Diseased Retina Seen through Neuron-Glia Interactions.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Mice LackingInternational journal of molecular sciences · 2022
    Article
  10. Article
  11. Article
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

10 authors at 2 institutions in 1 country.

Haruki TakeuchiGraduate School of Life Sciences, Ritsumeikan University, Kusatsu, Shiga, Japan.
Sho HorieCollege of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga, Japan.
Satoru MoritohCollege of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga, Japan.
Hiroki MatsushimaCollege of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga, Japan.
Tesshu HoriCollege of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Shiga, Japan.
Yoshitaka KimoriDepartment of Management and Information Sciences, Faculty of Environmental and Information Sciences, Fukui University of Technology, Fukui, Japan.
Katsunori KitanoCollege of Information Science and Engineering, Ritsumeikan University, Kusatsu, Shiga, Japan.ORCID 0000-0002-3209-6022
Yasuhiro TsuboCollege of Information Science and Engineering, Ritsumeikan University, Kusatsu, Shiga, Japan.
Masao TachibanaCenter for Systems Vision Science, Organization of Science and Technology, Ritsumeikan University, Kusatsu, Shiga, Japan.
Chieko KoikeGraduate School of Life Sciences, Ritsumeikan University, Kusatsu, Shiga, Japan.ORCID 0000-0002-1927-017X
Ritsumeikan University · JPFukui University of Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TRPM1, the first member of the melanoma-related transient receptor potential (TRPM) subfamily, is the visual transduction channel downstream of metabotropic glutamate receptor 6 (mGluR6) on retinal ON bipolar cells (BCs). Human TRPM1 mutations are associated with congenital stationary night blindness (CSNB). In both TRPM1 and mGluR6 KO mouse retinas, OFF but not ON BCs respond to light stimulation. Here we report an unexpected difference between TRPM1 knockout (KO) and mGluR6 KO mouse retinas. We used a multielectrode array (MEA) to record spiking in retinal ganglion cells (RGCs). We found spontaneous oscillations in TRPM1 KO retinas, but not in mGluR6 KO retinas. We performed a structural analysis on the synaptic terminals of rod ON BCs. Intriguingly, rod ON BC terminals were significantly smaller in TRPM1 KO retinas than in mGluR6 KO retinas. These data suggest that a deficiency of TRPM1, but not of mGluR6, in rod ON bipolar cells may affect synaptic terminal maturation. We speculate that impaired signaling between rod BCs and AII amacrine cells (ACs) leads to spontaneous oscillations. TRPM1 and mGluR6 are both essential components in the signaling pathway from photoreceptors to ON BC dendrites, yet they differ in their effects on the BC terminal and postsynaptic circuitry.

Indexed as

Amacrine CellsAnimalsDendritesEye Diseases, HereditaryGenetic Diseases, X-LinkedMiceMice, KnockoutMyopiaNight BlindnessReceptors, Metabotropic GlutamateRetinaRetinal Bipolar CellsRetinal Ganglion CellsSignal TransductionTRPM Cation Channelsmetabotropic glutamate receptor 6Receptors, Metabotropic GlutamateTrpm1 protein, mouseTRPM Cation Channels

Identifiers

PMID29854741
PMCPMC5964425
OpenAlexW2802866278

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.