Evidence map›Paper›PMID 20840468›Full record

ArticleBritish journal of pharmacology2011

Calcium signalling mediated through α7 and non-α7 nAChR stimulation is differentially regulated in bovine chromaffin cells to induce catecholamine release.

Laura del Barrio, Javier Egea, Rafael León, Alejandro Romero, Ana Ruiz, Mayte Montero, Javier Alvarez, Manuela G López

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Article
  8. Mitochondria as a possible target for nicotine action.Journal of bioenergetics and biomembranes · 2019
    Review
  9. Article
  10. Human nicotinic receptors in chromaffin cells: characterization and pharmacology.Pflugers Archiv : European journal of physiology · 2018
    Review
  11. Acetylcholine nicotinic receptor subtypes in chromaffin cells.Pflugers Archiv : European journal of physiology · 2018
    Review
  12. Review
  13. Review
  14. Microtubule dynamics at the growth cone are mediated by α7 nicotinic receptor activation of a Gαq and IP3 receptor pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  15. Review
  16. Article
  17. Article
  18. Presynaptic α7 nicotinic acetylcholine receptors enhance hippocampal mossy fiber glutamatergic transmission via PKA activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  19. Article
  20. 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

8 authors at 3 institutions in 1 country.

Laura del BarrioInstituto Teófilo Hernando, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain.
Javier Egea
Rafael León
Alejandro Romero
Ana Ruiz
Mayte Montero
Javier Alvarez
Manuela G López
Universidad Autónoma de Madrid · ESConsejo Superior de Investigaciones Científicas · ESInstituto de Biomedicina y Genética Molecular de Valladolid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeCa(2+) signalling and exocytosis mediated by nicotinic receptor (nAChR) subtypes, especially the α7 nAChR, in bovine chromaffin cells are still matters of debate. EXPERIMENTAL APPROACH: We have used chromaffin cell cultures loaded with Fluo-4 or transfected with aequorins directed to the cytosol or mitochondria, several nAChR agonists (nicotine, 5-iodo-A-85380, PNU282987 and choline), and the α7 nAChR allosteric modulator PNU120596. KEY

resultsMinimal [Ca(2+) ](c) transients, induced by low concentrations of selective α7 nAChR agonists and nicotine, were markedly increased by the α7 nAChR allosteric modulator PNU120596. These potentiated responses were completely blocked by the α7 nAChR antagonist α-bungarotoxin (α7-modulated-response). Conversely, high concentrations of the α7 nAChR agonists, nicotine or 5-iodo-A-85380 induced larger [Ca(2+) ](c) transients, that were blocked by mecamylamine but were unaffected by α-bungarotoxin (non-α7 response). [Ca(2+) ](c) increases mediated by α7 nAChR were related to Ca(2+) entry through non-L-type Ca(2+) channels, whereas non-α7 nAChR-mediated signals were related to L-type Ca(2+) channels; Ca(2+) -induced Ca(2+) -release contributed to both responses. Mitochondrial involvement in the control of [Ca(2+) ](c) transients, mediated by either receptor, was minimal. Catecholamine release coupled to α7 nAChRs was more efficient in terms of catecholamine released/[Ca(2+) ](c) . CONCLUSIONS AND IMPLICATIONS: [Ca(2+) ](c) and catecholamine release mediated by α7 nAChRs required an allosteric modulator and low doses of the agonist. At higher agonist concentrations, the α7 nAChR response was lost and the non-α7 nAChRs were activated. Catecholamine release might therefore be regulated by different nAChR subtypes, depending on agonist concentrations and the presence of allosteric modulators of α7 nAChRs.

Indexed as

Calcium SignalingAllosteric Regulationalpha7 Nicotinic Acetylcholine ReceptorAnimalsBenzamidesBridged Bicyclo CompoundsCatecholaminesCattleCells, CulturedCholineChromaffin CellsExocytosisFluorescent DyesNicotineNicotinic AgonistsReceptors, Nicotinicalpha7 Nicotinic Acetylcholine ReceptorBenzamidesBridged Bicyclo CompoundsCatecholaminesCholineFluorescent DyesNicotineNicotinic AgonistsPNU-282987Receptors, Nicotinic

Identifiers

PMID20840468
PMCPMC3012409
OpenAlexW1573628819

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.