Evidence map›Paper›PMID 20161791›Full record

ArticlePloS one2010

Ghrelin stimulation of growth hormone-releasing hormone neurons is direct in the arcuate nucleus.

Guillaume Osterstock, Pauline Escobar, Violeta Mitutsova, Laurie-Anne Gouty-Colomer, Pierre Fontanaud, François Molino, Jean-Alain Fehrentz, Danielle Carmignac, Jean Martinez, Nathalie C Guerineau and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-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

31 citing papers in PubMed, 75 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Hypothalamic GHRH.Reviews in endocrine & metabolic disorders · 2025
    Review
  6. Article
  7. Article
  8. Ghrelin receptor signaling in health and disease: a biased view.Trends in endocrinology and metabolism: TEM · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Omental transplantation for neuroendocrinological disorders.American journal of neurodegenerative disease · 2015
    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

13 authors at 5 institutions in 1 country.

Guillaume OsterstockInserm U-661, Montpellier, France.
Pauline Escobar
Violeta Mitutsova
Laurie-Anne Gouty-Colomer
Pierre Fontanaud
François Molino
Jean-Alain Fehrentz
Danielle Carmignac
Jean Martinez
Nathalie C Guerineau
Iain C A F Robinson
Patrice Mollard
Pierre-François Méry
Université de Montpellier · FRInserm · FRInstitut de Génomique Fonctionnelle · FRCentre National de la Recherche Scientifique · FRInstitut des Biomolécules Max Mousseron · FR

Funding

Medical Research Council MC_U117531708
6 · The paper itself

Abstract

backgroundGhrelin targets the arcuate nucleus, from where growth hormone releasing hormone (GHRH) neurones trigger GH secretion. This hypothalamic nucleus also contains neuropeptide Y (NPY) neurons which play a master role in the effect of ghrelin on feeding. Interestingly, connections between NPY and GHRH neurons have been reported, leading to the hypothesis that the GH axis and the feeding circuits might be co-regulated by ghrelin. PRINCIPAL

findingsHere, we show that ghrelin stimulates the firing rate of identified GHRH neurons, in transgenic GHRH-GFP mice. This stimulation is prevented by growth hormone secretagogue receptor-1 antagonism as well as by U-73122, a phospholipase C inhibitor and by calcium channels blockers. The effect of ghrelin does not require synaptic transmission, as it is not antagonized by gamma-aminobutyric acid, glutamate and NPY receptor antagonists. In addition, this hypothalamic effect of ghrelin is independent of somatostatin, the inhibitor of the GH axis, since it is also found in somatostatin knockout mice. Indeed, ghrelin does not modify synaptic currents of GHRH neurons. However, ghrelin exerts a strong and direct depolarizing effect on GHRH neurons, which supports their increased firing rate.

conclusionThus, GHRH neurons are a specific target for ghrelin within the brain, and not activated secondary to altered activity in feeding circuits. These results support the view that ghrelin related therapeutic approaches could be directed separately towards GH deficiency or feeding disorders.

Indexed as

Action PotentialsAnimalsArcuate Nucleus of HypothalamusCalcium Channel BlockersCalcium ChannelsDose-Response Relationship, DrugEstrenesFemaleGhrelinGreen Fluorescent ProteinsGrowth Hormone-Releasing HormoneIndolesMaleMiceMice, TransgenicNeurons1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dioneCalcium Channel BlockersCalcium ChannelsEstrenesGhrelinGreen Fluorescent Proteinsgrowth hormone releasing hexapeptideGrowth Hormone-Releasing HormoneIndolesmacimorelinOligopeptidesPyrrolidinonesReceptors, GhrelinTryptophanType C Phospholipases

Identifiers

PMID20161791
PMCPMC2820089
OpenAlexW2048505107

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.