Evidence map›Paper›PMID 26874559›Full record

ArticlePsychoneuroendocrinology2016

Ghrelin activates hypophysiotropic corticotropin-releasing factor neurons independently of the arcuate nucleus.

Agustina Cabral, Enrique Portiansky, Edith Sánchez-Jaramillo, Jeffrey M Zigman, Mario Perello

Open access · bronzeAbstract read
In one paragraph

Article in Psychoneuroendocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  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

5 authors at 3 institutions in 3 countries.

Agustina CabralLaboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology [IMBICE-Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)], La Plata, Buenos Aires, Argentina.
Enrique PortianskyImage Analysis Laboratory [School of Veterinary Sciences, National University of La Plata and CONICET], La Plata, Buenos Aires, Argentina.
Edith Sánchez-JaramilloDirección de Investigaciones en Neurociencias, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, México D.F., Mexico.
Jeffrey M ZigmanDepartment of Internal Medicine (Divisions of Hypothalamic Research and Endocrinology), Dallas, Texas, USA; Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Mario PerelloLaboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology [IMBICE-Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)], La Plata, Buenos Aires, Argentina. Electronic address: marioperello@yahoo.com.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz · MXThe University of Texas Southwestern Medical Center · US

Funding

Ghrelin's Role in MoodR01MH085298 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI ZIGMAN, JEFFREY M · 2010 to 2014
$2.0M
NIMH NIH HHS R01 MH085298NIMH NIH HHS R01MH085298
6 · The paper itself

Abstract

Previous work has established that the hormone ghrelin engages the hypothalamic-pituitary-adrenal neuroendocrine axis via activation of corticotropin-releasing factor (CRF) neurons of the hypothalamic paraventricular nucleus (PVN). The neuronal circuitry that mediates this effect of ghrelin is currently unknown. Here, we show that ghrelin-induced activation of PVN CRF neurons involved inhibition of γ-aminobutyric acid (GABA) inputs, likely via ghrelin binding sites that were localized at GABAergic terminals within the PVN. While ghrelin activated PVN CRF neurons in the presence of neuropeptide Y (NPY) receptor antagonists or in arcuate nucleus (ARC)-ablated mice, it failed to do it so in mice with ghrelin receptor expression limited to ARC agouti gene related protein (AgRP)/NPY neurons. These data support the notion that ghrelin activates PVN CRF neurons via inhibition of local GABAergic tone, in an ARC-independent manner. Furthermore, these data suggest that the neuronal circuits mediating ghrelin's orexigenic action vs. its role as a stress signal are anatomically dissociated.

Indexed as

AnimalsArcuate Nucleus of HypothalamusArginineCorticosteroneCorticotropin-Releasing HormoneGABA Antagonistsgamma-Aminobutyric AcidGene Knockdown TechniquesGhrelinInfusions, IntraventricularMaleMiceMuscimolNeuronsNeuropeptide YParaventricular Hypothalamic NucleusArginineBIBO 3304CorticosteroneCorticotropin-Releasing HormoneGABA Antagonistsgamma-Aminobutyric AcidGhrelinMuscimolNeuropeptide YReceptors, GhrelinGhrelinNeuropeptide Y (NPY)OrexigenicStressγ-Aminobutyric acid (GABA)

Identifiers

PMID26874559
PMCPMC4808343
OpenAlexW2254617479

What OpenQuestion holds

Textmetadata
LicenceTDM
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.