Persistent Disruption of a Traumatic Memory by Postretrieval Inactivation of Glucocorticoid Receptors in the Amygdala

Sophie Tronel, Cristina Alberini

Research output: Contribution to journalArticle

Abstract

Background: Posttraumatic stress disorder (PTSD) is characterized by acute and chronic changes in the stress response, which include alterations in glucocorticoid secretion and critically involve the limbic system, in particular the amygdala. Important symptoms of PTSD manifest as a classical conditioning to fear, which recurs each time trauma-related cues remind the subject of the original insult. Traumatic memories based on fear conditioning can be disrupted if interfering events or pharmacological interventions are applied following their retrieval. Methods and Results: Using an animal model, here we show that a traumatic memory is persistently disrupted if immediately after its retrieval glucocorticoid receptors are inactivated in the amygdala. The disruption of the memory is long lasting and memory retention does not re-emerge following strong reminders of the conditioned fear. Conclusions: We propose that a combinatorial approach of psychological and pharmacological intervention targeting the glucocorticoid system following memory retrieval may represent a novel direction for the treatment of PTSD.

Original languageEnglish (US)
Pages (from-to)33-39
Number of pages7
JournalBiological Psychiatry
Volume62
Issue number1
DOIs
StatePublished - Jul 1 2007

Fingerprint

Glucocorticoid Receptors
Amygdala
Post-Traumatic Stress Disorders
Fear
Glucocorticoids
Pharmacology
Limbic System
Classical Conditioning
Cues
Animal Models
Psychology
Wounds and Injuries

Keywords

  • Amygdala
  • animal model
  • fear memory
  • glucocorticoid receptor
  • PTSD
  • reconsolidation

ASJC Scopus subject areas

  • Biological Psychiatry

Cite this

Persistent Disruption of a Traumatic Memory by Postretrieval Inactivation of Glucocorticoid Receptors in the Amygdala. / Tronel, Sophie; Alberini, Cristina.

In: Biological Psychiatry, Vol. 62, No. 1, 01.07.2007, p. 33-39.

Research output: Contribution to journalArticle

@article{1b373d170cf243889c02d59241207f49,
title = "Persistent Disruption of a Traumatic Memory by Postretrieval Inactivation of Glucocorticoid Receptors in the Amygdala",
abstract = "Background: Posttraumatic stress disorder (PTSD) is characterized by acute and chronic changes in the stress response, which include alterations in glucocorticoid secretion and critically involve the limbic system, in particular the amygdala. Important symptoms of PTSD manifest as a classical conditioning to fear, which recurs each time trauma-related cues remind the subject of the original insult. Traumatic memories based on fear conditioning can be disrupted if interfering events or pharmacological interventions are applied following their retrieval. Methods and Results: Using an animal model, here we show that a traumatic memory is persistently disrupted if immediately after its retrieval glucocorticoid receptors are inactivated in the amygdala. The disruption of the memory is long lasting and memory retention does not re-emerge following strong reminders of the conditioned fear. Conclusions: We propose that a combinatorial approach of psychological and pharmacological intervention targeting the glucocorticoid system following memory retrieval may represent a novel direction for the treatment of PTSD.",
keywords = "Amygdala, animal model, fear memory, glucocorticoid receptor, PTSD, reconsolidation",
author = "Sophie Tronel and Cristina Alberini",
year = "2007",
month = "7",
day = "1",
doi = "10.1016/j.biopsych.2006.09.009",
language = "English (US)",
volume = "62",
pages = "33--39",
journal = "Biological Psychiatry",
issn = "0006-3223",
publisher = "Elsevier USA",
number = "1",

}

TY - JOUR

T1 - Persistent Disruption of a Traumatic Memory by Postretrieval Inactivation of Glucocorticoid Receptors in the Amygdala

AU - Tronel, Sophie

AU - Alberini, Cristina

PY - 2007/7/1

Y1 - 2007/7/1

N2 - Background: Posttraumatic stress disorder (PTSD) is characterized by acute and chronic changes in the stress response, which include alterations in glucocorticoid secretion and critically involve the limbic system, in particular the amygdala. Important symptoms of PTSD manifest as a classical conditioning to fear, which recurs each time trauma-related cues remind the subject of the original insult. Traumatic memories based on fear conditioning can be disrupted if interfering events or pharmacological interventions are applied following their retrieval. Methods and Results: Using an animal model, here we show that a traumatic memory is persistently disrupted if immediately after its retrieval glucocorticoid receptors are inactivated in the amygdala. The disruption of the memory is long lasting and memory retention does not re-emerge following strong reminders of the conditioned fear. Conclusions: We propose that a combinatorial approach of psychological and pharmacological intervention targeting the glucocorticoid system following memory retrieval may represent a novel direction for the treatment of PTSD.

AB - Background: Posttraumatic stress disorder (PTSD) is characterized by acute and chronic changes in the stress response, which include alterations in glucocorticoid secretion and critically involve the limbic system, in particular the amygdala. Important symptoms of PTSD manifest as a classical conditioning to fear, which recurs each time trauma-related cues remind the subject of the original insult. Traumatic memories based on fear conditioning can be disrupted if interfering events or pharmacological interventions are applied following their retrieval. Methods and Results: Using an animal model, here we show that a traumatic memory is persistently disrupted if immediately after its retrieval glucocorticoid receptors are inactivated in the amygdala. The disruption of the memory is long lasting and memory retention does not re-emerge following strong reminders of the conditioned fear. Conclusions: We propose that a combinatorial approach of psychological and pharmacological intervention targeting the glucocorticoid system following memory retrieval may represent a novel direction for the treatment of PTSD.

KW - Amygdala

KW - animal model

KW - fear memory

KW - glucocorticoid receptor

KW - PTSD

KW - reconsolidation

UR - http://www.scopus.com/inward/record.url?scp=34250199393&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34250199393&partnerID=8YFLogxK

U2 - 10.1016/j.biopsych.2006.09.009

DO - 10.1016/j.biopsych.2006.09.009

M3 - Article

VL - 62

SP - 33

EP - 39

JO - Biological Psychiatry

JF - Biological Psychiatry

SN - 0006-3223

IS - 1

ER -