Evidence map›Paper›PMID 23840801›Full record

ArticlePloS one2013

Presynaptic Localization and Possible Function of Calcium-Activated Chloride Channel Anoctamin 1 in the Mammalian Retina.

Ji Hyun Jeon, Sun Sook Paik, Myung-Hoon Chun, Uhtaek Oh, In-Beom Kim

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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  5. Reduced Expression of TMEM16A Impairs Nitric Oxide-Dependent ClFrontiers in cellular neuroscience · 2022
    Article
  6. Article
  7. Article
  8. Contributions of glutamate transporters and CaExperimental eye research · 2019
    Article
  9. Review
  10. Modulating Ca²⁺ signals: a common theme for TMEM16, Ist2, and TMC.Pflugers Archiv : European journal of physiology · 2016
    Review
  11. Article
  12. Four basic residues critical for the ion selectivity and pore blocker sensitivity of TMEM16A calcium-activated chloride channels.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  13. Article
  14. Article
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  17. 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

5 authors at 2 institutions in 1 country.

Ji Hyun JeonDepartment of Anatomy, College of Medicine, The Catholic University of Korea, Seoul, Korea ; Catholic Neuroscience Institute, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Sun Sook Paik
Myung-Hoon Chun
Uhtaek Oh
In-Beom Kim
Catholic University of Korea · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium (Ca(2+))-activated chloride (Cl(-)) channels (CaCCs) play a role in the modulation of action potentials and synaptic responses in the somatodendritic regions of central neurons. In the vertebrate retina, large Ca(2+)-activated Cl(-) currents (ICl(Ca)) regulate synaptic transmission at photoreceptor terminals; however, the molecular identity of CaCCs that mediate ICl(Ca) remains unclear. The transmembrane protein, TMEM16A, also called anoctamin 1 (ANO1), has been recently validated as a CaCC and is widely expressed in various secretory epithelia and nervous tissues. Despite the fact that tmem16a was first cloned in the retina, there is little information on its cellular localization and function in the mammalian retina. In this study, we found that ANO1 was abundantly expressed as puncta in 2 synaptic layers. More specifically, ANO1 immunoreactivity was observed in the presynaptic terminals of various retinal neurons, including photoreceptors. ICl(Ca) was first detected in dissociated rod bipolar cells expressing ANO1. ICl(Ca) was abolished by treatment with the Ca(2+) channel blocker Co(2+), the L-type Ca(2+) channel blocker nifedipine, and the Cl(-) channel blockers 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and niflumic acid (NFA). More specifically, a recently discovered ANO1-selective inhibitor, T16Ainh-A01, and a neutralizing antibody against ANO1 inhibited ICl(Ca) in rod bipolar cells. Under a current-clamping mode, the suppression of ICl(Ca) by using NPPB and T16Ainh-A01 caused a prolonged Ca(2+) spike-like depolarization evoked by current injection in dissociated rod bipolar cells. These results suggest that ANO1 confers ICl(Ca) in retinal neurons and acts as an intrinsic regulator of the presynaptic membrane potential during synaptic transmission.

Indexed as

Action PotentialsAnimalsAnoctamin-1CalciumChloride ChannelsMaleMiceMice, Inbred C57BLPatch-Clamp TechniquesPresynaptic TerminalsRetinaSynaptic TransmissionANO1 protein, mouseAnoctamin-1CalciumChloride Channels

Identifiers

PMID23840801
PMCPMC3693959
OpenAlexW2077131634

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.