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

Sophie Tronel, Cristina M. Alberini
Biological Psychiatry. 2007-07-01; 62(1): 33-39
DOI: 10.1016/j.biopsych.2006.09.009

PubMed
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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.

 

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