Persistent disruption of a traumatic memory by postretrieval inactivation of glucocorticoid receptors in the amygdala.
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.


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.
Tronel
Sophie
S
Department of Neuroscience, Mount Sinai School of Medicine, New York, New York 10029, USA. Cristina.Alberini@mssm.edu
Alberini
Cristina M
CM
D000679:Amygdala / Q000503:physiopathology*; D000818:Animals; D003214:Conditioning, Classical / Q000502:physiology; D004195:Disease Models, Animal; D005239:Fear / Q000502:physiology; D006801:Humans; D008569:Memory Disorders / Q000503:physiopathology*; D011939:Mental Recall / Q000502:physiology*; D011965:Receptors, Glucocorticoid / Q000502:physiology*; D013313:Stress Disorders, Post-Traumatic / Q000503:physiopathology / Q000523:psychology* / Q000628:therapy
D011965:Receptors, Glucocorticoid