Evidence map›Paper›PMID 25430741›Full record

ArticleThe EMBO journal2015

A secretagogin locus of the mammalian hypothalamus controls stress hormone release.

Roman A Romanov, Alán Alpár, Ming-Dong Zhang, Amit Zeisel, André Calas, Marc Landry, Matthew Fuszard, Sally L Shirran, Robert Schnell, Árpád Dobolyi and 12 more

Abstract read
In one paragraph

Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
–field-weighted citation impact
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

49 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Neuronal activity modulates the expression of secretagogin, a CaActa physiologica (Oxford, England) · 2025
    Article
  10. Review
  11. Article
  12. Review
  13. A hydrophobic groove in secretagogin allows for alternate interactions with SNAP-25 and syntaxin-4 in endocrine tissues.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Article
  15. Article
  16. SCGN deficiency is a risk factor for autism spectrum disorder.Signal transduction and targeted therapy · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. 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

22 authors.

Roman A RomanovDepartment of Medical Biochemistry & Biophysics, Karolinska Institutet, Stockholm, Sweden Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Alán AlpárDepartment of Medical Biochemistry & Biophysics, Karolinska Institutet, Stockholm, Sweden alpar.alan@med.semmelweis-univ.hu Tibor.Harkany@ki.se.
Ming-Dong ZhangDepartment of Medical Biochemistry & Biophysics, Karolinska Institutet, Stockholm, Sweden Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Amit ZeiselDepartment of Medical Biochemistry & Biophysics, Karolinska Institutet, Stockholm, Sweden.
André CalasLaboratory for Central Mechanisms of Pain Sensitization, Interdisciplinary Institute for Neuroscience, CNRS UMR 5297 Université Bordeaux 2, Bordeaux, France.
Marc LandryLaboratory for Central Mechanisms of Pain Sensitization, Interdisciplinary Institute for Neuroscience, CNRS UMR 5297 Université Bordeaux 2, Bordeaux, France.
Matthew FuszardSchool of Chemistry, University of St. Andrews, St. Andrews, UK.
Sally L ShirranSchool of Chemistry, University of St. Andrews, St. Andrews, UK.
Robert SchnellDepartment of Medical Biochemistry & Biophysics, Karolinska Institutet, Stockholm, Sweden.
Árpád DobolyiDepartment of Anatomy, Semmelweis University, Budapest, Hungary.
Márk OláhDepartment of Human Morphology and Developmental Biology, Semmelweis University, Budapest, Hungary.
Lauren SpenceInstitute of Medical Sciences, University of Aberdeen, Aberdeen, UK.
Jan MulderDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
Henrik MartensSynaptic Systems GmbH, Göttingen, Germany.
Miklós PalkovitsHuman Brain Tissue Bank and Laboratory, Semmelweis University, Budapest, Hungary.
Mathias UhlenScience for Life Laboratory, Albanova University Center, Royal Institute of Technology, Stockholm, Sweden.
Harald H SitteCenter for Physiology and Pharmacology, Institute of Pharmacology Medical University of Vienna, Vienna, Austria.
Catherine H BottingSchool of Chemistry, University of St. Andrews, St. Andrews, UK.
Ludwig WagnerUniversity Clinic for Internal Medicine III General Hospital Vienna, Vienna, Austria.
Sten LinnarssonDepartment of Medical Biochemistry & Biophysics, Karolinska Institutet, Stockholm, Sweden.
Tomas HökfeltDepartment of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Tibor HarkanyDepartment of Medical Biochemistry & Biophysics, Karolinska Institutet, Stockholm, Sweden Department of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, Vienna, Austria alpar.alan@med.semmelweis-univ.hu Tibor.Harkany@ki.se.

Funding

Wellcome TrustWellcome Trust 094476/Z/10/Z
6 · The paper itself

Abstract

A hierarchical hormonal cascade along the hypothalamic-pituitary-adrenal axis orchestrates bodily responses to stress. Although corticotropin-releasing hormone (CRH), produced by parvocellular neurons of the hypothalamic paraventricular nucleus (PVN) and released into the portal circulation at the median eminence, is known to prime downstream hormone release, the molecular mechanism regulating phasic CRH release remains poorly understood. Here, we find a cohort of parvocellular cells interspersed with magnocellular PVN neurons expressing secretagogin. Single-cell transcriptome analysis combined with protein interactome profiling identifies secretagogin neurons as a distinct CRH-releasing neuron population reliant on secretagogin's Ca(2+) sensor properties and protein interactions with the vesicular traffic and exocytosis release machineries to liberate this key hypothalamic releasing hormone. Pharmacological tools combined with RNA interference demonstrate that secretagogin's loss of function occludes adrenocorticotropic hormone release from the pituitary and lowers peripheral corticosterone levels in response to acute stress. Cumulatively, these data define a novel secretagogin neuronal locus and molecular axis underpinning stress responsiveness.

Indexed as

AnimalsCorticosteroneCorticotropin-Releasing HormoneMaleMiceNeuronsParaventricular Hypothalamic NucleusPituitary GlandRNA InterferenceSecretagoginsStress, PhysiologicalTranscriptomeCorticosteroneCorticotropin-Releasing HormoneSCGN protein, mouseSecretagoginsacute stressCa2+ sensorHPA axisvesicular release

Identifiers

PMID25430741
PMCPMC4291479

What OpenQuestion holds

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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.