Evidence map›Paper›PMID 17082234›Full record

ArticleThe Journal of physiology2007

Subunit-specific modulation of T-type calcium channels by zinc.

Achraf Traboulsie, Jean Chemin, Marc Chevalier, Jean-François Quignard, Joël Nargeot, Philippe Lory

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Impact of Retinal Degeneration on Response of ON and OFF Cone Bipolar Cells to Electrical Stimulation.IEEE transactions on neural systems and rehabilitation engineering : a publication of the IEEE Engineering in Medicine and Biology Society · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. CaChannels (Austin, Tex.) · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Neuronal Cav3 channelopathies: recent progress and perspectives.Pflugers Archiv : European journal of physiology · 2020
    Review
  14. Article
  15. Delineating an extracellular redox-sensitive module in T-type CaThe Journal of biological chemistry · 2020
    Article
  16. Review
  17. Article
  18. Zinc transporters and dysregulated channels in cancers.Frontiers in bioscience (Landmark edition) · 2017
    Review
  19. Article
  20. Review
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

6 authors at 4 institutions in 1 country.

Achraf TraboulsieDépartement de Physiologie, Institut de Génomique Fonctionnelle (IGF), CNRS UMR 5203, INSERM U661, Universités de Montpellier I and II, 141 rue de la Cardonille, 34094 Montpellier cedex 05, France.
Jean Chemin
Marc Chevalier
Jean-François Quignard
Joël Nargeot
Philippe Lory
Institut de Génomique Fonctionnelle · FRCentre National de la Recherche Scientifique · FRInserm · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc (Zn2+) functions as a signalling molecule in the nervous system and modulates many ionic channels. In this study, we have explored the effects of Zn2+ on recombinant T-type calcium channels (CaV3.1, CaV3.2 and CaV3.3). Using tsA-201 cells, we demonstrate that CaV3.2 current (IC50, 0.8 microm) is significantly more sensitive to Zn2+ than are CaV3.1 and CaV3.3 currents (IC50, 80 microm and approximately 160 microm, respectively). This inhibition of CaV3 currents is associated with a shift to more negative membrane potentials of both steady-state inactivation for CaV3.1, CaV3.2 and CaV3.3 and steady-state activation for CaV3.1 and CaV3.3 currents. We also document changes in kinetics, especially a significant slowing of the inactivation kinetics for CaV3.1 and CaV3.3, but not for CaV3.2 currents. Notably, deactivation kinetics are significantly slowed for CaV3.3 current (approximately 100-fold), but not for CaV3.1 and CaV3.2 currents. Consequently, application of Zn2+ results in a significant increase in CaV3.3 current in action potential clamp experiments, while CaV3.1 and CaV3.2 currents are significantly reduced. In neuroblastoma NG 108-15 cells, the duration of CaV3.3-mediated action potentials is increased upon Zn2+ application, indicating further that Zn2+ behaves as a CaV3.3 channel opener. These results demonstrate that Zn2+ exhibits differential modulatory effects on T-type calcium channels, which may partly explain the complex features of Zn2+ modulation of the neuronal excitability in normal and disease states.

Indexed as

Calcium Channel BlockersAction PotentialsAlgorithmsCalcium Channels, T-TypeCell LineCell Line, TumorElectrophysiologyHumansMembrane Transport ProteinsPatch-Clamp TechniquesRecombinant ProteinsSynaptic TransmissionThalamusTransfectionZincCACNA1G protein, humanCACNA1H protein, humanCACNA1I protein, humanCalcium Channel BlockersCalcium Channels, T-TypeMembrane Transport ProteinsRecombinant ProteinsZinc

Identifiers

PMID17082234
PMCPMC2075129
OpenAlexW1540396301

What OpenQuestion holds

Textmetadata
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.