Evidence map›Paper›PMID 25004388›Full record

ArticleTranslational psychiatry2014

Central anandamide deficiency predicts stress-induced anxiety: behavioral reversal through endocannabinoid augmentation.

R J Bluett, J C Gamble-George, D J Hermanson, N D Hartley, L J Marnett, S Patel

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
12.4field-weighted citation impact, top 1% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. The effects of FAAH inhibition on the neural basis of anxiety-related processing in healthy male subjects: a randomized clinical trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Trial
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  17. Endocannabinoid signaling in stress, nausea, and vomiting.Neurogastroenterology and motility · 2025
    Review
  18. Pharmaceuticals (Basel, Switzerland) · 2025
    Article
  19. Article
  20. Article

28 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

6 authors at 1 institution in 1 country.

R J Bluett1] Department of Psychiatry, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA [2] Vanderbilt Brain Institute, Vanderbilt University Medical Center, Nashville, TN, USA.
J C Gamble-George1] Department of Psychiatry, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA [2] Vanderbilt Brain Institute, Vanderbilt University Medical Center, Nashville, TN, USA.
D J HermansonA.B. Hancock Jr. Memorial Laboratory for Cancer Research, Departments of Biochemistry, Chemistry, and Pharmacology, Vanderbilt Institute of Chemical Biology, Center in Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
N D HartleyDepartment of Psychiatry, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
L J MarnettA.B. Hancock Jr. Memorial Laboratory for Cancer Research, Departments of Biochemistry, Chemistry, and Pharmacology, Vanderbilt Institute of Chemical Biology, Center in Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
S Patel1] Department of Psychiatry, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA [2] Vanderbilt Brain Institute, Vanderbilt University Medical Center, Nashville, TN, USA [3] Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Vanderbilt University Medical Center · US

Funding

THE PHARMACOLOGY OF INHIBITORS OF HEME PROTEIN-CATALYZED LIPID PEROXIDATIONP50GM015431 · NIGMS · VANDERBILT UNIVERSITY · PI CAPRIOLI, RICHARD M · 1985 to 2010
$15.0M
Vanderbilt/Meharry Initiative for Minority Student DvptR25GM062459 · NIGMS · VANDERBILT UNIVERSITY · PI VELEZ EDWARDS, DIGNA R · 2002 to 2020
$10.4M
Therapeutic Modulation of Endothelial Cell TetrahydrobiopterinP01GM015431 · NIGMS · VANDERBILT UNIVERSITY · PI ROBERTS, JACKSON L · 2011 to 2015
$9.5M
Training in Fundamental NeuroscienceT32MH064913 · NIMH · VANDERBILT UNIVERSITY · PI IHRIE, REBECCA A, WINDER, DANNY G. · 2001 to 2022
$7.6M
Substrate-selective inhibition of COX-2 to target affective disordersR01MH100096 · NIMH · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PATEL, SACHIN · 2013 to 2018
$2.4M
Stress adaptations in endocannabinoid signaling in the amygdalaK08MH090412 · NIMH · VANDERBILT UNIVERSITY · PI PATEL, SACHIN · 2010 to 2014
$842k
(R)-flurbiprofen Substrate-Selective Inhibition of COX-2 and Analog DevelopmentF31DA031572 · NIDA · VANDERBILT UNIVERSITY · PI HERMANSON, DANIEL · 2011 to 2013
$107k
NIDA NIH HHS DA031572NIDA NIH HHS F31 DA031572NIGMS NIH HHS GM15431NIGMS NIH HHS P01 GM015431NIGMS NIH HHS P50 GM015431NIGMS NIH HHS R25 GM062459NIMH NIH HHS K08 MH090412NIMH NIH HHS MH064913NIMH NIH HHS MH090412NIMH NIH HHS MH100096NIMH NIH HHS R01 MH100096NIMH NIH HHS T32 MH064913
6 · The paper itself

Abstract

Stress is a major risk factor for the development of mood and anxiety disorders; elucidation of novel approaches to mitigate the deleterious effects of stress could have broad clinical applications. Pharmacological augmentation of central endogenous cannabinoid (eCB) signaling may be an effective therapeutic strategy to mitigate the adverse behavioral and physiological consequences of stress. Here we show that acute foot-shock stress induces a transient anxiety state measured 24 h later using the light-dark box assay and novelty-induced hypophagia test. Acute pharmacological inhibition of the anandamide-degrading enzyme, fatty acid amide hydrolase (FAAH), reverses the stress-induced anxiety state in a cannabinoid receptor-dependent manner. FAAH inhibition does not significantly affect anxiety-like behaviors in non-stressed mice. Moreover, whole brain anandamide levels are reduced 24 h after acute foot-shock stress and are negatively correlated with anxiety-like behavioral measures in the light-dark box test. These data indicate that central anandamide levels predict acute stress-induced anxiety, and that reversal of stress-induced anandamide deficiency is a key mechanism subserving the therapeutic effects of FAAH inhibition. These studies provide further support that eCB-augmentation is a viable pharmacological strategy for the treatment of stress-related neuropsychiatric disorders.

Indexed as

AmidohydrolasesAnimalsAnxietyArachidonic AcidsBehavior, AnimalDisease Models, AnimalEndocannabinoidsFatty Acid Amide HydrolasesMaleMiceMice, Inbred ICRPolyunsaturated AlkamidesStress, PsychologicalAmidohydrolasesanandamideArachidonic AcidsEndocannabinoidsFatty Acid Amide HydrolasesPolyunsaturated Alkamides

Identifiers

PMID25004388
PMCPMC4119220
OpenAlexW2050990247

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.