Evidence map›Paper›PMID 23363338›Full record

ArticleJournal of neuroendocrinology2013

Involvement of prolactin-releasing peptide in the activation of oxytocin neurones in response to food intake.

M Yamashita, Y Takayanagi, M Yoshida, K Nishimori, M Kusama, T Onaka

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuroendocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Role of Oxytocin in Obesity.Current diabetes reports · 2026
    Review
  3. Review
  4. Article
  5. Review
  6. Morpho-Electric Properties and Diversity of Oxytocin Neurons in Paraventricular Nucleus of Hypothalamus in Female and Male Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  7. Roles of Oxytocin in Stress Responses, Allostasis and Resilience.International journal of molecular sciences · 2021
    Review
  8. Do oxytocin neurones affect feeding?Journal of neuroendocrinology · 2021
    Review
  9. Review
  10. Article
  11. Oxytocin as an Anti-obesity Treatment.Frontiers in neuroscience · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Metabolic Effects of Oxytocin.Endocrine reviews · 2020
    Review
  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

6 authors at 2 institutions in 1 country.

M YamashitaDivision of Brain and Neurophysiology, Department of Physiology, Jichi Medical University, Shimotsuke-shi, Japan.
Y Takayanagi
M Yoshida
K Nishimori
M Kusama
T Onaka
Jichi Medical University · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Food intake activates neurones expressing prolactin-releasing peptide (PrRP) in the medulla oblongata and oxytocin neurones in the hypothalamus. Both PrRP and oxytocin have been shown to have an anorexic action. In the present study, we investigated whether the activation of oxytocin neurones following food intake is mediated by PrRP. We first examined the expression of PrRP receptors (also known as GPR10) in rats. Immunoreactivity of PrRP receptors was observed in oxytocin neurones and in vasopressin neurones in the paraventricular and supraoptic nuclei of the hypothalamus and in the bed nucleus of the stria terminalis. Application of PrRP to isolated supraoptic nuclei facilitated the release of oxytocin and vasopressin. In mice, re-feeding increased the expression of Fos protein in oxytocin neurones of the hypothalamus and bed nucleus of the stria terminalis. The increased expression of Fos protein in oxytocin neurones following re-feeding or i.p. administration of cholecystokinin octapeptide (CCK), a peripheral satiety factor, was impaired in PrRP-deficient mice. CCK-induced oxytocin increase in plasma was also impaired in PrRP-deficient mice. Furthermore, oxytocin receptor-deficient mice showed an increased meal size, as reported in PrRP-deficient mice and in CCKA receptor-deficient mice. These findings suggest that PrRP mediates, at least in part, the activation of oxytocin neurones in response to food intake, and that the CCK-PrRP-oxytocin pathway plays an important role in the control of the termination of each meal.

Indexed as

Feeding BehaviorAnimalsMaleNeuronsOxytocinProlactin-Releasing HormoneRatsRats, WistarOxytocinProlactin-Releasing Hormone

Identifiers

PMID23363338
PMCPMC3664423
OpenAlexW2080320459

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.