Evidence map›Paper›PMID 26257395›Full record

ArticleGenes, brain, and behavior2015

Angiotensin type 1a receptors on corticotropin-releasing factor neurons contribute to the expression of conditioned fear.

R C Hurt, J C Garrett, O P Keifer, A Linares, L Couling, R C Speth, K J Ressler, P J Marvar

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Genes, brain, and behavior, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02709018 (Enhancing Fear Extinction Via Angiotensin Type 1 Receptor Inhibition), which is not on this map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 18% 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.

NCT02709018 nacompletednot on this mapstarted 2016, after this paper: background citation

Enhancing Fear Extinction Via Angiotensin Type 1 Receptor Inhibition: A Randomized Controlled Trial in Posttraumatic Stress Disorder

TypeinterventionalSponsorUniversity of California, San DiegoRan2016 to 2020Enrolled149ConditionsPosttraumatic Stress DisorderArmslosartan, Placebo
3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Enhancing Fear Extinction: Pharmacological Approaches.Current topics in behavioral neurosciences · 2023
    Article
  5. Article
  6. Review
  7. Review
  8. Limbic Neuropeptidergic Modulators of Emotion and Their Therapeutic Potential for Anxiety and Post-Traumatic Stress Disorder.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. A Unique "Angiotensin-Sensitive" Neuronal Population Coordinates Neuroendocrine, Cardiovascular, and Behavioral Responses to Stress.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  15. Amygdala-Dependent Molecular Mechanisms of the Tac2 Pathway in Fear Learning.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016
    Article
  16. Article
  17. Autonomic and inflammatory consequences of posttraumatic stress disorder and the link to cardiovascular disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
    Review
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

8 authors at 5 institutions in 2 countries.

R C HurtDepartment of Psychiatry and Behavioral Sciences, Emory University School of Medicine.
J C GarrettDepartment of Psychiatry and Behavioral Sciences, Emory University School of Medicine.
O P KeiferDepartment of Psychiatry and Behavioral Sciences, Emory University School of Medicine.
A LinaresFarquhar College of Arts and Sciences.
L CoulingDepartment of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL.
R C SpethDepartment of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL.
K J ResslerDepartment of Psychiatry and Behavioral Sciences, Emory University School of Medicine.
P J MarvarDepartment of Pharmacology and Physiology, The George Washington University School of Medical and Health Sciences, Washington, DC, USA.
Hizen Psychiatric Center · JPNova Southeastern University · USEmory National Primate Research CenterGeorgetown University · USGeorge Washington University · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI Louis M Weiner · 1990 to 2026
$71.5M
Maternal Morbidity and Mortality: Risk Factors, Early Detection and Personalized InterventionUL1TR001409 · NCATS · GEORGETOWN UNIVERSITY · PI GONDRE-LEWIS, MARJORIE C, MELLMAN, THOMAS A · 2015 to 2024
$37.8M
MEDICAL SCIENTIST TRAINING PROGRAMT32GM008169 · NIGMS · EMORY UNIVERSITY · PI GROSS, ROBERT E · 1987 to 2021
$20.3M
Georgetown-Howard Universities Center for Clinical and Translational Science (GHUUL1TR000101 · NCATS · GEORGETOWN UNIVERSITY · PI MELLMAN, THOMAS A, VERBALIS, JOSEPH G · 2012 to 2015
$19.3M
ENNCF - Viral Vector CoreP30NS055077 · NINDS · EMORY UNIVERSITY · PI LEVEY, ALLAN I · 2008 to 2018
$6.8M
Stress-induced hypertension and the role of the neuroimmune systemR00HL107675 · NHLBI · GEORGE WASHINGTON UNIVERSITY · PI MARVAR, PAUL J · 2014 to 2016
$746k
NCATS NIH HHS 8 UL1 TR000101NCATS NIH HHS UL1 TR000101NCATS NIH HHS UL1 TR001409NCI NIH HHS P30 CA051008NCI NIH HHS P30 CA51008NHLBI NIH HHS R00 HL107675NHLBI NIH HHS R00 HL107675-03NIGMS NIH HHS T32 GM008169NINDS NIH HHS P30 NS055077
6 · The paper itself

Abstract

Although generally associated with cardiovascular regulation, angiotensin II receptor type 1a (AT1a R) blockade in mouse models and humans has also been associated with enhanced fear extinction and decreased post-traumatic stress disorder (PTSD) symptom severity, respectively. The mechanisms mediating these effects remain unknown, but may involve alterations in the activities of corticotropin-releasing factor (CRF)-expressing cells, which are known to be involved in fear regulation. To test the hypothesis that AT1a R signaling in CRFergic neurons is involved in conditioned fear expression, we generated and characterized a conditional knockout mouse strain with a deletion of the AT1a R gene from its CRF-releasing cells (CRF-AT1a R((-/-)) ). These mice exhibit normal baseline heart rate, blood pressure, anxiety and locomotion, and freeze at normal levels during acquisition of auditory fear conditioning. However, CRF-AT1a R((-/-)) mice exhibit less freezing than wild-type mice during tests of conditioned fear expression-an effect that may be caused by a decrease in the consolidation of fear memory. These results suggest that central AT1a R activity in CRF-expressing cells plays a role in the expression of conditioned fear, and identify CRFergic cells as a population on which AT1 R antagonists may act to modulate fear extinction.

Indexed as

Conditioning, ClassicalFearAnimalsCorticotropin-Releasing HormoneFreezing Reaction, CatalepticMaleMiceNeuronsReceptor, Angiotensin, Type 1Agtr1a protein, mouseCorticotropin-Releasing HormoneReceptor, Angiotensin, Type 1Amygdalaangiotensin IIangiotensin II receptor type 1blood pressurecardiovascularcorticotropin-releasing factorextinctionfearparaventricular nucleusPTSD

Identifiers

PMID26257395
PMCPMC4573765
OpenAlexW1952608928

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.