Evidence map›Paper›PMID 22530815›Full record

ReviewGenes, brain, and behavior2012

Fear extinction and BDNF: translating animal models of PTSD to the clinic.

R Andero, K J Ressler

Open access · greenAbstract readReview
In one paragraph

Review in Genes, brain, and behavior, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 2 pooled it
9.4field-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

127 citing papers in PubMed, 2 syntheses or guidelines pooled it, 272 citations in OpenAlex.

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  16. PDE4B Missense Variant Increases Susceptibility to Post-traumatic Stress Disorder-Relevant Phenotypes in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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67 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

2 authors at 1 institution in 1 country.

R AnderoDepartment of Psychiatry and Behavioral Sciences, Yerkes National Primate Research Center, Emory University School of Medicine, Atlanta, GA, USA.
K J Ressler
Emory University · US

Funding

Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
Genetic and Trauma-Related Risk Factors for PTSDR01MH071537 · NIMH · EMORY UNIVERSITY · PI RESSLER, KERRY J. · 2005 to 2014
$8.5M
Genetic and estrogen-dependent regulation of the human PAC1R receptor and PTSDR01MH096764 · NIMH · MCLEAN HOSPITAL · PI RESSLER, KERRY J. · 2012 to 2016
$2.1M
Molecular Regulation of GABA(A) Receptor Function in AmygdalaR01DA019624 · NIDA · EMORY UNIVERSITY · PI RESSLER, KERRY J. · 2006 to 2010
$1.8M
Prefrontal Cortex BDNF and Amygdala-Dependent Emotional LearningChallenge Area:RC1MH088467 · NIMH · EMORY UNIVERSITY · PI RESSLER, KERRY J. · 2009 to 2010
$782k
Synaptic Plasticity and Extinction of FearK01MH069884 · NIMH · EMORY UNIVERSITY · PI RESSLER, KERRY J · 2004 to 2007
$654k
The role of cortical BDNF in the regulation of fear conditioning and extinctionF32MH085443 · NIMH · EMORY UNIVERSITY · PI CHOI, DENNIS CLARENCE · 2009 to 2011
$157k
NIDA NIH HHS R01DA01962NIDA NIH HHS R01 DA019624NIH HHS P51 OD011132NIH HHS P51OD11132NIMH NIH HHS F32 MH085443NIMH NIH HHS F32MH085443NIMH NIH HHS K01 MH069884NIMH NIH HHS R01 MH071537NIMH NIH HHS R01 MH096764NIMH NIH HHS RC1 MH088467
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) is the most studied neurotrophin involved in synaptic plasticity processes that are required for long-term learning and memory. Specifically, BDNF gene expression and activation of its high-affinity tropomyosin-related kinase B (TrkB) receptor are necessary in the amygdala, hippocampus and prefrontal cortex for the formation of emotional memories, including fear memories. Among the psychiatric disorders with altered fear processing, there is post-traumatic stress disorder (PTSD) which is characterized by an inability to extinguish fear memories. Since BDNF appears to enhance extinction of fear, targeting impaired extinction in anxiety disorders such as PTSD via BDNF signalling may be an important and novel way to enhance treatment efficacy. The aim of this review is to provide a translational point of view that stems from findings in the BDNF regulation of synaptic plasticity and fear extinction. In addition, there are different systems that seem to alter fear extinction through BDNF modulation like the endocannabinoid system and the hypothalamic-pituitary adrenal axis. Recent work also finds that the pituitary adenylate cyclase-activating polypeptide and PAC1 receptor, which are upstream of BDNF activation, may be implicated in PTSD. Especially interesting are data that exogenous fear extinction enhancers such as antidepressants, histone deacetylases inhibitors and D-cycloserine, a partial N-methyl d-aspartate agonist, may act through or in concert with the BDNF-TrkB system. Finally, we review studies where recombinant BDNF and a putative TrkB agonist, 7,8-dihydroxyflavone, may enhance extinction of fear. These approaches may lead to novel agents that improve extinction in animal models and eventually humans.

Indexed as

Disease Models, AnimalAnimalsBrainBrain-Derived Neurotrophic FactorExtinction, PsychologicalFearHumansLearningNeuronal PlasticityStress Disorders, Post-TraumaticTranslational Research, BiomedicalBrain-Derived Neurotrophic Factor

Identifiers

PMID22530815
PMCPMC3389160
OpenAlexW2073927880

What OpenQuestion holds

Textmetadata
LicenceTDM
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.