Evidence map›Paper›PMID 26578878›Full record

ArticleFrontiers in molecular neuroscience2015

Selective potentiation of alpha 1 glycine receptors by ginkgolic acid.

Galyna Maleeva, Svetlana Buldakova, Piotr Bregestovski

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
6.4field-weighted citation impact, top 5% 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

4 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016
    Review
  4. 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

3 authors at 2 institutions in 2 countries.

Galyna MaleevaAix Marseille Université, INS UMR_S 1106 Marseille, France ; INSERM, UMR_S 1106 Marseille, France ; Department of Cytology, Bogomoletz Institute of Physiology Kyiv, Ukraine.
Svetlana BuldakovaAix Marseille Université, INS UMR_S 1106 Marseille, France ; INSERM, UMR_S 1106 Marseille, France.
Piotr BregestovskiAix Marseille Université, INS UMR_S 1106 Marseille, France ; INSERM, UMR_S 1106 Marseille, France.
Inserm · FRAix-Marseille Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycine receptors (GlyRs) belong to the superfamily of pentameric cys-loop receptor-operated channels and are involved in numerous physiological functions, including movement, vision, and pain. In search for compounds performing subunit-specific modulation of GlyRs we studied action of ginkgolic acid, an abundant Ginkgo biloba product. Using patch-clamp recordings, we analyzed the effects of ginkgolic acid in concentrations from 30 nM to 25 μM on α1-α3 and α1/β, α2/β configurations of GlyR and on GABAARs expressed in cultured CHO-K1 cells and mouse neuroblastoma (N2a) cells. Ginkgolic acid caused an increase in the amplitude of currents mediated by homomeric α1 and heteromeric α1/β GlyRs and provoked a left-shift of the concentration-dependent curves for glycine. Even at high concentrations (10-25 μM) ginkgolic acid was not able to augment ionic currents mediated by α2, α2/β, and α3 GlyRs, or by GABAAR consisting of α1/β2/γ2 subunits. Mutation of three residues (T59A/A261G/A303S) in the α2 GlyR subunit to the corresponding ones from the α1 converted the action of ginkgolic acid to potentiation with a distinct decrease in EC50 for glycine, suggesting an important role for these residues in modulation by ginkgolic acid. Our results suggest that ginkgolic acid is a novel selective enhancer of α1 GlyRs.

Indexed as

CHO cellsglycine receptorion currentsligand-gated channelspatch clampwhole-cell recording

Identifiers

PMID26578878
PMCPMC4624854
OpenAlexW1833855516

What OpenQuestion holds

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Registered trials

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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.