Background
Paradoxical changes in memory represent a troublesome characteristic of posttraumatic
stress disorder (PTSD). Exceptionally vivid intrusive memories of some aspects of
the trauma are mingled with patchy amnesia regarding other important aspects. Molecular
studies of the memory process suggest that the conversion from labile short-term memory
into long-term fixed traces involves protein synthesis. This study assessed the effects
of administration of anisomycin, a protein synthesis inhibitor, after initial exposure,
after exposure to a cue associated with triggering experience, and after reexposure
to the triggering trauma in an animal model of PTSD.
Method
Magnitude of changes in prevalence of anxiety-like behaviors on the elevated plus-maze
and nonhabituated exaggerated startle reaction were compared in rats that were exposed
to predator stress, with and without microinjection of anisomycin.
Results
Microinjection of anisomycin before and after stress exposure reduced anxiety-like
and avoidant behavior, reduced the mean startle amplitude, and reversed the stress-induced
habituation deficit 7 days later. The persistent anxiety-like behaviors that were
seen after stress exposure do not appear to be sensitive to anisomycin after reexposure
to a cue associated with the event or after reexposure to the index experience.
Conclusions
Disruption of the process of traumatic memory consolidation may be useful for mitigating
PTSD symptoms.
Key Words
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Article info
Publication history
Published online: May 30, 2006
Accepted:
March 6,
2006
Received in revised form:
September 5,
2005
Received:
April 7,
2005
Identification
Copyright
© 2006 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.