Evidence map›Paper›PMID 28260504›Full record

ReviewCurrent molecular pharmacology2018

The CRF Family of Neuropeptides and their Receptors - Mediators of the Central Stress Response.

Nina Dedic, Alon Chen, Jan M Deussing

Open access · greenAbstract readReview
In one paragraph

Review in Current molecular pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 184 citations in OpenAlex.

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  12. Deep phenotyping reveals CRH and FKBP51-dependent behavioral profiles following chronic social stress exposure in male mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  13. PACAP regulates neuroendocrine and behavioral stress responses via CRF-containing neurons of the rat hypothalamic paraventricular nucleus.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  14. Lateral olivocochlear neurons modulate cochlear responses to noise exposure.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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26 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Nina DedicDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Kraepelinstr, 2-10, 80804 Munich. Germany.
Alon ChenDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Kraepelinstr, 2-10, 80804 Munich. Germany.
Jan M DeussingDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Kraepelinstr, 2-10, 80804 Munich. Germany.
Max Planck Institute of Psychiatry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDysregulated stress neurocircuits, caused by genetic and/or environmental changes, underlie the development of many neuropsychiatric disorders. Corticotropin-releasing factor (CRF) is the major physiological activator of the hypothalamic-pituitary-adrenal (HPA) axis and consequently a primary regulator of the mammalian stress response. Together with its three family members, urocortins (UCNs) 1, 2, and 3, CRF integrates the neuroendocrine, autonomic, metabolic and behavioral responses to stress by activating its cognate receptors CRFR1 and CRFR2.

objectiveHere we review the past and current state of the CRF/CRFR field, ranging from pharmacological studies to genetic mouse models and virus-mediated manipulations.

resultsAlthough it is well established that CRF/CRFR1 signaling mediates aversive responses, including anxiety and depression-like behaviors, a number of recent studies have challenged this viewpoint by revealing anxiolytic and appetitive properties of specific CRF/CRFR1 circuits. In contrast, the UCN/CRFR2 system is less well understood and may possibly also exert divergent functions on physiology and behavior depending on the brain region, underlying circuit, and/or experienced stress conditions.

conclusionA plethora of available genetic tools, including conventional and conditional mouse mutants targeting CRF system components, has greatly advanced our understanding about the endogenous mechanisms underlying HPA system regulation and CRF/UCN-related neuronal circuits involved in stress-related behaviors. Yet, the detailed pathways and molecular mechanisms by which the CRF/UCN-system translates negative or positive stimuli into the final, integrated biological response are not completely understood. The utilization of future complementary methodologies, such as cell-type specific Cre-driver lines, viral and optogenetic tools will help to further dissect the function of genetically defined CRF/UCN neurocircuits in the context of adaptive and maladaptive stress responses.

Indexed as

Stress, PhysiologicalAnimalsCorticotropin-Releasing HormoneGenetic EngineeringHumansReceptors, Corticotropin-Releasing HormoneSignal TransductionVirusesCorticotropin-Releasing HormoneReceptors, Corticotropin-Releasing HormoneCorticotropin-releasing factorhypothalamic-pituitary-adrenal (HPA)mouse genetic toolsneuropsychiatric disordersstressurocortin

Identifiers

PMID28260504
PMCPMC5930453
OpenAlexW2594351553

What OpenQuestion holds

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LicenceCC BY-NC
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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.