Evidence map›Paper›PMID 33151288›Full record

ArticleThe international journal of neuropsychopharmacology2021

PI3K-Akt Signaling in the Basolateral Amygdala Facilitates Traumatic Stress Enhancements in Fear Memory.

Dayan Knox, Rebecca Della Valle, Negin Mohammadmirzaei, Brianna Shultz, Matt Biddle, Abigail Farkash, Marisa Chamness, Emily Moulton

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The international journal of neuropsychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

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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 1 institution in 1 country.

Dayan KnoxDepartment of Psychological and Brain Sciences, University of Delaware, Newark, Delaware, USA.
Rebecca Della ValleDepartment of Psychological and Brain Sciences, University of Delaware, Newark, Delaware, USA.
Negin MohammadmirzaeiDepartment of Psychological and Brain Sciences, University of Delaware, Newark, Delaware, USA.
Brianna ShultzDepartment of Psychological and Brain Sciences, University of Delaware, Newark, Delaware, USA.
Matt BiddleDepartment of Psychological and Brain Sciences, University of Delaware, Newark, Delaware, USA.
Abigail FarkashDepartment of Psychological and Brain Sciences, University of Delaware, Newark, Delaware, USA.
Marisa ChamnessDepartment of Psychological and Brain Sciences, University of Delaware, Newark, Delaware, USA.
Emily MoultonDepartment of Psychological and Brain Sciences, University of Delaware, Newark, Delaware, USA.
University of Delaware · US

Funding

Updated confocal microscope in the Imaging Core facility to support biomedical researchP20GM103653 · NIGMS · DELAWARE STATE UNIVERSITY · PI HARRINGTON, MELISSA A · 2012 to 2022
$22.7M
NIGMS NIH HHS P20 GM103653
6 · The paper itself

Abstract

backgroundA core symptom of posttraumatic stress disorder is persistent fear memory, which can be defined as fear memory that is resistant to updating, inhibition, or extinction. posttraumatic stress disorder emerges after traumatic stress exposure, but neurobiological mechanisms via which traumatic stress leads to persistent fear memory are not well defined. Akt signaling within the amygdala (Amy) is enhanced with traumatic stress, and phosphatidylinositol kinase 3 (PI3K) activation of Akt within the basolateral Amy (BLA) has been implicated as critical to fear memory formation. These findings raise the possibility that traumatic stress enhances PI3K→Akt signaling in the BLA, which leads to persistent fear memory.

methodsTo test this hypothesis, rats were exposed to traumatic stress using the single prolonged stress model, and changes in Akt phosphorylation were assayed in the Amy at 0 and 30 minutes after fear conditioning (FC). In a separate experiment, we inhibited PI3K→Akt signaling in the BLA prior to FC and observed the effect this had on acquisition, expression, and extinction of FC in stressed and control rats.

resultsEnhanced Akt phosphorylation in the Amy at both time points was observed in stressed rats, but not in control rats. PI3K→Akt inhibition in the BLA had no effect on freezing in control rats but decreased freezing during extinction training and testing in stressed rats.

conclusionThese findings suggest that PI3K→Akt signaling in the BLA could be a mechanism via which traumatic stress leads to fear memory that is resistant to extinction.

Indexed as

Basolateral Nuclear ComplexExtinction, PsychologicalMental RecallStress Disorders, Post-TraumaticStress, PsychologicalAnimalsBehavior, AnimalDisease Models, AnimalFearMalePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktBasolateral amygdalaextinctionfear memoryPTSDsingle prolonged stress

Identifiers

PMID33151288
PMCPMC7968623
OpenAlexW3097370478

What OpenQuestion holds

Textmetadata
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.