Evidence map›Paper›PMID 16798884›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Deletion of the neuropeptide Y (NPY) Y1 receptor gene reveals a regulatory role of NPY on catecholamine synthesis and secretion.

Cláudia Cavadas, Daniel Céfai, Joana Rosmaninho-Salgado, Maria Augusta Vieira-Coelho, Eduardo Moura, Nathalie Busso, Thierry Pedrazzini, Daniela Grand, Samuel Rotman, Bernard Waeber and 2 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 56 citations in OpenAlex.

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  11. Fasting induces a form of autonomic synaptic plasticity that prevents hypoglycemia.Proceedings of the National Academy of Sciences of the United States of America · 2016
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  14. Neuropeptide y gates a stress-induced, long-lasting plasticity in the sympathetic nervous system.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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

12 authors at 6 institutions in 4 countries.

Cláudia Cavadas*Center for Neurosciences and Cell Biology and Faculty of Pharmacy, University of Coimbra, 3004-517 Coimbra, Portugal.
Daniel CéfaiDepartment of Medicine, Divisions of.
Joana Rosmaninho-Salgado*Center for Neurosciences and Cell Biology and Faculty of Pharmacy, University of Coimbra, 3004-517 Coimbra, Portugal.
Maria Augusta Vieira-CoelhoInstitute of Pharmacology and Therapeutics, Faculty of Medicine, 4200-319 Porto, Portugal.
Eduardo MouraInstitute of Pharmacology and Therapeutics, Faculty of Medicine, 4200-319 Porto, Portugal.
Nathalie BussoRheumatology.
Thierry PedrazziniDepartment of Medicine, Divisions of.
Daniela GrandClinical Pharmacology and Toxicology, and.
Samuel RotmanInstitute of Pathology, Centre Hospitalier Universaire Vaudois, 1011 Lausanne, Switzerland; and.
Bernard Waeber**Clinical Pathophysiology, and.
Jean-François AubertDepartment of Medicine, Divisions of.
Eric GrouzmannClinical Pharmacology and Toxicology, and eric.grouzmann@chuv.hospvd.ch.
Division of Chemistry · USInstituto Português de Oncologia Francisco Gentil · PTUniversity of Coimbra · PTCenter for Rheumatology · USResearch Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences · RUUniversity Hospital of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The contribution of neuropeptide Y (NPY), deriving from adrenal medulla, to the adrenosympathetic tone is unknown. We found that in response to NPY, primary cultures of mouse adrenal chromaffin cells secreted catecholamine, and that this effect was abolished in cultures from NPY Y(1) receptor knockout mice (Y(1)-/-). Compared with wild-type mice (Y(1)+/+), the adrenal content and constitutive release of catecholamine were increased in chromaffin cells from Y(1)-/- mice. In resting animals, catecholamine plasma concentrations were higher in Y(1)-/- mice. Comparing the adrenal glands of both genotypes, no differences were observed in the area of the medulla, cortex, and X zone. The high turnover of adrenal catecholamine in Y(1)-/- mice was explained by the enhancement of tyrosine hydroxylase (TH) activity, although no change in the affinity of the enzyme was observed. The molecular interaction between the Y(1) receptor and TH was demonstrated by the fact that NPY markedly inhibited the forskolin-induced luciferin activity in Y(1) receptor-expressing SK-N-MC cells transfected with a TH promoter sequence. We propose that NPY controls the release and synthesis of catecholamine from the adrenal medulla and consequently contributes to the sympathoadrenal tone.

Indexed as

Gene DeletionAdrenal GlandsAnimalsCatecholaminesCells, CulturedChromaffin CellsEpinephrineFemaleMaleMiceMice, KnockoutNeuropeptide YNorepinephrinePromoter Regions, GeneticReceptors, Neuropeptide YRNA, MessengerCatecholaminesEpinephrineNeuropeptide Yneuropeptide Y-Y1 receptorNorepinephrineReceptors, Neuropeptide YRNA, MessengerTyrosine 3-Monooxygenase

Identifiers

PMID16798884
PMCPMC1502486
OpenAlexW2084287610

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.