Evidence map›Paper›PMID 24055593›Full record

ArticleNeurobiology of learning and memory2014

Extinguishing trace fear engages the retrosplenial cortex rather than the amygdala.

Janine L Kwapis, Timothy J Jarome, Jonathan L Lee, Marieke R Gilmartin, Fred J Helmstetter

Abstract read
In one paragraph

Article in Neurobiology of learning and memory, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

50 citing papers in PubMed, 67 citations in OpenAlex.

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  10. Medial Amygdalar Tau Is Associated With Mood Symptoms in Preclinical Alzheimer's Disease.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2024
    Article
  11. Article
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  15. Article
  16. Retrosplenial cortex and aversive conditioning.Frontiers in behavioral neuroscience · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Janine L KwapisDepartment of Psychology, University of Wisconsin-Milwaukee, 2441 E. Hartford Ave., Milwaukee, WI 53211, USA.
Timothy J JaromeDepartment of Psychology, University of Wisconsin-Milwaukee, 2441 E. Hartford Ave., Milwaukee, WI 53211, USA.
Jonathan L LeeDepartment of Psychology, University of Wisconsin-Milwaukee, 2441 E. Hartford Ave., Milwaukee, WI 53211, USA.
Marieke R GilmartinDepartment of Psychology, University of Wisconsin-Milwaukee, 2441 E. Hartford Ave., Milwaukee, WI 53211, USA.
Fred J HelmstetterDepartment of Psychology, University of Wisconsin-Milwaukee, 2441 E. Hartford Ave., Milwaukee, WI 53211, USA. Electronic address: fjh@uwm.edu.
University of Wisconsin–Milwaukee · US

Funding

Distributed synaptic plasticity in fear conditioningR01MH069558 · NIMH · UNIVERSITY OF WISCONSIN MILWAUKEE · PI HELMSTETTER, FRED J · 2005 to 2014
$2.9M
Prefrontal interactions with hippocampus and amygdala during trace fearR03MH090426 · NIMH · UNIVERSITY OF WISCONSIN MILWAUKEE · PI HELMSTETTER, FRED J · 2010 to 2011
$144k
The role of protein kinase Mzeta in hippocampal-dependent memory maintenance.F31MH090685 · NIMH · UNIVERSITY OF WISCONSIN MILWAUKEE · PI KWAPIS, JANINE LYNN · 2010 to 2013
$126k
NIMH NIH HHS F31 MH090685NIMH NIH HHS F31MH090685NIMH NIH HHS R01 MH069558NIMH NIH HHS R01MH069558NIMH NIH HHS R03 MH090426
6 · The paper itself

Abstract

Extinction learning underlies the treatment for a variety of anxiety disorders. Most of what is known about the neurobiology of extinction is based on standard "delay" fear conditioning, in which awareness is not required for learning. Little is known about how complex, explicit associations extinguish, however. "Trace" conditioning is considered to be a rodent model of explicit fear because it relies on both the cortex and hippocampus and requires explicit contingency awareness in humans. Here, we explore the neural circuit supporting trace fear extinction in order to better understand how complex memories extinguish. We first show that the amygdala is selectively involved in delay fear extinction; blocking intra-amygdala glutamate receptors disrupted delay, but not trace extinction. Further, ERK phosphorylation was increased in the amygdala after delay, but not trace extinction. We then identify the retrosplenial cortex (RSC) as a key structure supporting trace extinction. ERK phosphorylation was selectively increased in the RSC following trace extinction and blocking intra-RSC NMDA receptors impaired trace, but not delay extinction. These findings indicate that delay and trace extinction require different neural circuits; delay extinction requires plasticity in the amygdala whereas trace extinction requires the RSC. Anxiety disorders linked to explicit memory may therefore depend on cortical processes that have not been traditionally targeted by extinction studies based on delay fear.

Indexed as

AmygdalaAnimalsBehavior, AnimalCerebral CortexConditioning, PsychologicalExtinction, PsychologicalExtracellular Signal-Regulated MAP KinasesFearMaleRatsRats, Long-EvansReceptors, N-Methyl-D-AspartateValine2-amino-5-phosphopentanoic acidExtracellular Signal-Regulated MAP KinasesReceptors, N-Methyl-D-AspartateValineAPVDelay fear conditioningERKExtinctionNMDATrace fear conditioning

Identifiers

PMID24055593
PMCPMC3959632
OpenAlexW2037607749

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.