Evidence map›Paper›PMID 28805209›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2018

Neuropeptide S Induces Acute Anxiolysis by Phospholipase C-Dependent Signaling within the Medial Amygdala.

Thomas Grund, Inga D Neumann

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Neuropeptide S Activates Paraventricular Oxytocin Neurons to Induce Anxiolysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
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.

Thomas GrundDepartment of Behavioural and Molecular Neurobiology, University of Regensburg, Regensburg, Germany.
Inga D NeumannDepartment of Behavioural and Molecular Neurobiology, University of Regensburg, Regensburg, Germany.
University of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuropeptide S (NPS) is an important anxiolytic substance of the brain. However, the signaling pathways downstream of NPS receptor (NPSR) activation, underlying the behavioral effect of NPS, remain largely unknown. Here, we show that bilateral microinfusion of NPS (0.2 nmol/0.5 μl) into the medial amygdala (MeA) of male adult Wistar rats reduced anxiety-related behavior on both the elevated plus-maze and the open field. Moreover, as shown in amygdala tissue micropunches intracerebroventricular infusion of NPS (1 nmol/5 μl) (1) evoked phosphorylation and synthesis of CaMKIIα in relation to reference protein β-tubulin representing Ca

Indexed as

AmygdalaAnimalsAnti-Anxiety AgentsCalcium-Calmodulin-Dependent Protein Kinase KinaseDideoxyadenosineEstrenesExploratory BehaviorInfusions, IntraventricularMaleMaze LearningMicroinjectionsMitogen-Activated Protein Kinase 3NeuropeptidesPhosphorylationPyrrolidinonesRats1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dioneAnti-Anxiety AgentsCalcium-Calmodulin-Dependent Protein Kinase KinaseDideoxyadenosineEstrenesMitogen-Activated Protein Kinase 3Neuropeptidesneuropeptide S, ratPyrrolidinonesType C Phospholipases

Identifiers

PMID28805209
PMCPMC5854792
OpenAlexW2746974727

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.