Evidence map›Paper›PMID 17664345›Full record

ArticleThe Journal of general physiology2007

Modulation of extracellular proton fluxes from retinal horizontal cells of the catfish by depolarization and glutamate.

Matthew A Kreitzer, Leon P Collis, Anthony J A Molina, Peter J S Smith, Robert Paul Malchow

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

30 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
  3. ATP-mediated increase in HJournal of neurophysiology · 2024
    Article
  4. Extracellular ATP-Induced Alterations in Extracellular HFrontiers in cellular neuroscience · 2021
    Article
  5. Article
  6. Article
  7. Localizing Proton-Mediated Inhibitory Feedback at the Retinal Horizontal Cell-Cone Synapse with Genetically-Encoded pH Probes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Autocrine boost of NMDAR current in hippocampal CA1 pyramidal neurons by a PMCA-dependent, perisynaptic, extracellular pH shift.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  16. Article
  17. Article
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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 4 institutions in 1 country.

Matthew A KreitzerDepartment of Biology, Indiana Wesleyan University, Marion, IN 46953, USA. matthew.kreitzer@indwes.edu
Leon P Collis
Anthony J A Molina
Peter J S Smith
Robert Paul Malchow
Marine Biological Laboratory · USBoston University · USIndiana Wesleyan University · USU.S. National Science Foundation · US

Funding

VOLTAMMETRIC DETECTION OF METAL IONSP41RR001395 · NCRR · MARINE BIOLOGICAL LABORATORY · PI SMITH, PETER JS · 1985 to 2010
$12.7M
NCRR NIH HHS P41 RR 001395NCRR NIH HHS P41 RR001395
6 · The paper itself

Abstract

Self-referencing H(+)-selective microelectrodes were used to measure extracellular proton fluxes from cone-driven horizontal cells isolated from the retina of the catfish (Ictalurus punctatus). The neurotransmitter glutamate induced an alkalinization of the area adjacent to the external face of the cell membrane. The effect of glutamate occurred regardless of whether the external solution was buffered with 1 mM HEPES, 3 mM phosphate, or 24 mM bicarbonate. The AMPA/kainate receptor agonist kainate and the NMDA receptor agonist N-methyl-D-aspartate both mimicked the effect of glutamate. The effect of kainate on proton flux was inhibited by the AMPA/kainate receptor blocker CNQX, and the effect of NMDA was abolished by the NMDA receptor antagonist DAP-5. Metabotropic glutamate receptor agonists produced no alteration in proton fluxes from horizontal cells. Depolarization of cells either by increasing extracellular potassium or directly by voltage clamp also produced an alkalinization adjacent to the cell membrane. The effects of depolarization on proton flux were blocked by 10 microM nifedipine, an inhibitor of L-type calcium channels. The plasmalemma Ca(2+/)H(+) ATPase (PMCA) blocker 5(6)-carboxyeosin also significantly reduced proton flux modulation by glutamate. Our results are consistent with the hypothesis that glutamate-induced extracellular alkalinizations arise from activation of the PMCA pump following increased intracellular calcium entry into cells. This process might help to relieve suppression of photoreceptor neurotransmitter release that results from exocytosed protons from photoreceptor synaptic terminals. Our findings argue strongly against the hypothesis that protons released by horizontal cells act as the inhibitory feedback neurotransmitter that creates the surround portion of the receptive fields of retinal neurons.

Indexed as

ProtonsAnimalsCalciumCatfishesExcitatory Amino Acid AgonistsGlutamic AcidHydrogen-Ion ConcentrationKainic AcidMembrane PotentialsMicroelectrodesN-MethylaspartatePatch-Clamp TechniquesPotassiumRetinal Horizontal CellsSodium-Hydrogen ExchangersCalciumExcitatory Amino Acid AgonistsGlutamic AcidKainic AcidN-MethylaspartatePotassiumProtonsSodium-Hydrogen Exchangers

Identifiers

PMID17664345
PMCPMC2151636
OpenAlexW2071805663

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.