Evidence map›Paper›PMID 20853513›Full record

ArticleThe Journal of comparative neurology2010

Tuberoinfundibular peptide of 39 residues modulates the mouse hypothalamic-pituitary-adrenal axis via paraventricular glutamatergic neurons.

Eugene Dimitrov, Ted Björn Usdin

Open access · greenAbstract read
In one paragraph

Article in The Journal of comparative neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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  14. Molecular and functional diversity of GABA-A receptors in the enteric nervous system of the mouse colon.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  15. Neuropathic and inflammatory pain are modulated by tuberoinfundibular peptide of 39 residues.Proceedings of the National Academy of Sciences of the United States of America · 2013
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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

2 authors at 1 institution in 1 country.

Eugene DimitrovSection on Fundamental Neuroscience, National Institute of Mental Health, Bethesda, Maryland 20892, USA.
Ted Björn Usdin
National Institute of Mental Health · US

Funding

Peptide Receptor SystemsZIAMH002685 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI USDIN, TED B · 2009 to 2016
$10.0M
Intramural NIH HHS ZIA MH002685NIMH NIH HHS ZIA MH002685-16
6 · The paper itself

Abstract

Neurons in the subparafascicular area at the caudal border of the thalamus that contain the neuropeptide tuberoinfundibular peptide of 39 residues (TIP39) densely innervate several hypothalamic areas, including the paraventricular nucleus (PVN). These areas contain a matching distribution of TIP39's receptor, the parathyroid hormone receptor 2 (PTH2R). Frequent PTH2R coexpression with a vesicular glutamate transporter (VGlut2) suggests that TIP39 could presynaptically regulate glutamate release. By using immunohistochemistry we found CRH-ir neurons surrounded by PTH2R-ir fibers and TIP39-ir axonal projections in the PVN area of the mouse brain. Labeling hypothalamic neuroendocrine neurons by peripheral injection of fluorogold in PTH2R-lacZ knock-in mice showed that most PTH2Rs are on PVN and peri-PVN interneurons and not on neuroendocrine cells. Double fluorescent in situ hybridization revealed a high level of coexpression between PTH2R and VGlut2 mRNA by cells located in the PVN and nearby brain areas. Local TIP39 infusion (100 pmol) robustly increased pCREB-ir in the PVN and adjacent perinuclear zone. It also increased plasma corticosterone and decreased plasma prolactin. These effects of TIP39 on pCREB-ir, corticosterone, and prolactin were abolished by coinfusion of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and DL-2-amino-5-phosphonopentanoic acid (AP-5; 30 pmol each) and were absent in PTH2R knockout mice. Basal plasma corticosterone was slightly decreased in TIP39 knockout mice just before onset of their active phase. The present data indicate that the TIP39 ligand/PTH2 receptor system provides facilitatory regulation of the hypothalamic-pituitary-adrenal axis via hypothalamic glutamatergic neurons and that it may regulate other neuroendocrine systems by a similar mechanism.

Indexed as

AnimalsCorticosteroneCorticotropin-Releasing HormoneGlutamic AcidHumansHypothalamo-Hypophyseal SystemMiceMice, Inbred C57BLMice, KnockoutNeuronsNeuropeptidesParaventricular Hypothalamic NucleusPituitary-Adrenal SystemReceptor, Parathyroid Hormone, Type 2Vesicular Glutamate Transport Protein 2CorticosteroneCorticotropin-Releasing HormoneGlutamic AcidNeuropeptidesReceptor, Parathyroid Hormone, Type 2tuberoinfundibular peptide 39Vesicular Glutamate Transport Protein 2

Identifiers

PMID20853513
PMCPMC3004125
OpenAlexW2038901410

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.