Evidence map›Paper›PMID 21940450›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Relief of Mg²⁺-dependent inhibition of TRPM1 by PKCα at the rod bipolar cell synapse.

Melissa Ann F Rampino, Scott A Nawy

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. The Retinal Light Response Is Modulated by an mGluR5-Mediated Retrograde Signal from ON-Bipolar Cells to Photoreceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  2. Article
  3. The Variety of Mechanosensitive Ion Channels in Retinal Neurons.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Review
  6. PKC regulation of ion channels: The involvement of PIPThe Journal of biological chemistry · 2022
    Review
  7. Review
  8. Article
  9. Review
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  11. Article
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  14. Review
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  19. G-protein-mediated inhibition of the Trp channel TRPM1 requires the Gβγ dimer.Proceedings of the National Academy of Sciences of the United States of America · 2012
    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

2 authors at 1 institution in 1 country.

Melissa Ann F RampinoDominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA. melissaann.rampino@phd.einstein.yu.edu
Scott A Nawy
Albert Einstein College of Medicine · US

Funding

MECHANISMS OF SYNAPTIC TRANSMISSION IN THE RETINAR01EY010254 · NEI · YESHIVA UNIVERSITY · PI NAWY, SCOTT · 1993 to 2013
$4.2M
NEI NIH HHS EY010254NEI NIH HHS R01 EY010254
6 · The paper itself

Abstract

In the retina, light onset hyperpolarizes photoreceptors and depolarizes ON bipolar cells at the sign inverting photoreceptor-ON bipolar cell synapse. Transmission at this synapse is mediated by a signaling cascade comprised of mGluR6, a G-protein containing G(αo), and the cation channel TRP melastatin 1 (TRPM1). This system is thought to be common to both the rod- and ON-cone-driven pathways, which control vision under scotopic and photopic conditions, respectively. In this study, we present evidence that the rod pathway is uniquely susceptible to modulation by PKCα at the rod-rod bipolar cell synapse. Decreased production of DAG (an activator of PKC) by inhibition of PIP₂ (phosphatidylinositol-4,5-bisphosphate) hydrolysis caused depression of the TRPM1 current. Conversely, addition of a DAG analog, 2-acetyl-1-oleoyl-sn-glycerol (OAG), potentiated the current in rod bipolar cells but not in ON-cone bipolar cells. The potentiating effects of OAG were absent both in mutant mice that lack PKCα expression and in wild-type mice in which enzymatic activity of PKCα was pharmacologically inhibited. In addition, we found that, like other members of the TRPM subfamily, TRPM1 current is susceptible to voltage-independent inhibition by intracellular magnesium, and that modulation by PKCα relieves this inhibition, as the potentiating effects of OAG are absent in low intracellular magnesium. We conclude that activation of PKCα initiates a modulatory mechanism at the rod-rod bipolar cell synapse whose function is to reduce inhibition of the TRPM1 current by magnesium, thereby increasing the gain of transmission at this synapse.

Indexed as

AnimalsDiglyceridesEnzyme InhibitorsFemaleIn Vitro TechniquesMagnesiumMembrane PotentialsMiceMice, Mutant StrainsPhosphatidylinositol 4,5-DiphosphatePhospholipase DProtein Kinase C-alphaRetinal Bipolar CellsRetinal Cone Photoreceptor CellsRetinal Rod Photoreceptor CellsSynapses1-oleoyl-2-acetoyl-sn-glycerolDiglyceridesEnzyme InhibitorsMagnesiumPhosphatidylinositol 4,5-DiphosphatePhospholipase DProtein Kinase C-alphaTRPM Cation Channels

Identifiers

PMID21940450
PMCPMC3189818
OpenAlexW2049478406

What OpenQuestion holds

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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.