Evidence map›Paper›PMID 11784782›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

Modulatory mechanism of the endogenous peptide catestatin on neuronal nicotinic acetylcholine receptors and exocytosis.

Carlos J Herrero, Eva Alés, Antonio J Pintado, Manuela G López, Esther García-Palomero, Sushil K Mahata, Daniel T O'Connor, Antonio G García, Carmen Montiel

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. The Role of Catestatin in Preeclampsia.International journal of molecular sciences · 2024
    Review
  3. Serum Catestatin Level as a Stratification Assessment Tool in Non-Critical COVID-19 Patients.International journal of environmental research and public health · 2023
    Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Chromogranin A: a novel susceptibility gene for essential hypertension.Cellular and molecular life sciences : CMLS · 2010
    Review
  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

9 authors at 2 institutions in 2 countries.

Carlos J HerreroDepartamento de Farmacologia and Instituto Teófilo Hernando, Facultad de Medicina, Universidad Autónoma de Madrid, 28029 Madrid, Spain.
Eva Alés
Antonio J Pintado
Manuela G López
Esther García-Palomero
Sushil K Mahata
Daniel T O'Connor
Antonio G García
Carmen Montiel
Universidad Autónoma de Madrid · ESUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The catestatin fragment of chromogranin A is the first known endogenous compound able to inhibit catecholamine release elicited by the activation of neuronal nicotinic acetylcholine receptors (nAChRs) of different animal species and catecholaminergic cell types. However, how catestatin regulates the receptor activity, which subunit combination of the heteropentameric forms of receptor is better blocked by the peptide, or how it affects the different stages of the exocytotic process have not yet been evaluated. To address these questions, we have assayed the effects of catestatin: (first) on the inward currents elicited by ACh (I(ACh)) in voltage-clamped oocytes expressing different combinations of nAChR subunits; and (second) on the cytosolic Ca2+ concentration, [Ca2+]c, and quantal release of catecholamines simultaneously monitored in single adrenal chromaffin cells stimulated with ACh. Catestatin potently blocks all the subtypes of nAChRs studied. Furthermore, it inhibits the alpha3beta4 current in a reversible, noncompetitive, voltage-, and use-dependent manner, a behavior compatible with open-channel blockade. In fura-2-loaded single chromaffin cells, the peptide reduced the [Ca2+]c signal and the total release of catecholamines elicited by ACh; however, catestatin did not modify the kinetics or the last step of the exocytotic process. Our results suggest that catestatin might play an autocrine regulatory role in neuroendocrine secretion through its interaction with different native nAChR subtypes; the extent of receptor blockade by the peptide could be acutely regulated by the intensity and duration of the presynaptic stimulus.

Indexed as

AcetylcholineAnimalsCalciumCatecholaminesCattleCell LineChromaffin CellsChromogranin AChromograninsDose-Response Relationship, DrugExocytosisIon TransportMembrane FusionMembrane PotentialsMicroinjectionsOocytesAcetylcholineCalciumCatecholaminesChromogranin Achromogranin A (344-364)ChromograninsPeptide FragmentsProtein SubunitsReceptors, Nicotinic

Identifiers

PMID11784782
PMCPMC6758662
OpenAlexW1903774592

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.