Program#/Poster#: |
616.01/XX21 |
Title: |
Neuroimaging assessment
of the mechanisms underlying behavioral interference of reconsolidation
in humans |
Location: |
Hall A-C |
Presentation Time: |
Tuesday, Nov 15, 2011,
8:00 AM - 9:00 AM |
Authors: |
*J. W. KANEN1,
D. SCHILLER3, J. E. LEDOUX2,4, M. H. MONFILS5,
E. A. PHELPS1,2,4;
1Dept. of Psychology, 2Ctr. for Neural Sci., New York
Univ., New York, NY; 3Departments of Psychiatry and Neurosci.,
Mount Sinai Med. Sch., New York, NY; 4Nathan S. Kline Inst. for
Psychiatric Res., Orangeburg, NY; 5Dept. of Psychology, Univ.
of Texas, Austin, TX |
Abstract: |
Recent research in humans
and rodents has shown that introducing safety information through extinction
training during the reconsolidation of conditioned fear persistently alters
the fear memory representation and prevents the return of fear. In humans
this change in fear memories has been shown to last at least one year, consistent
with the idea that fear memory representation in the amygdala is significantly
altered. The behavioral results to date, however, cannot verify the purported
neural effects. If reconsolidation alters an amygdala dependent memory representation,
this should be reflected in activity in brain systems linked to conditioned
fear and extinction. Here we used a non-invasive technique to target the
reconsolidation of fear memories, in conjunction with human functional neuroimaging.
Healthy participants underwent classical fear conditioning to create two
mild fear memories, assessed by skin conductance response and amygdala activity.
Two conditioned stimuli (CS+) were partially reinforced by the receipt of
an aversive electric shock, or unconditioned stimulus (US), while a third
conditioned stimulus (CS-) never predicted the US. A day later, subjects
underwent extinction training during which the two CS+s were repeatedly
presented without the US. Ten minutes prior to extinction, one of the two
fear memories was reactivated by brief non-reinforced presentation of one
CS+. This allowed a direct comparison of the neural mechanisms of extinction
with and without reconsolidation update, within subjects. Twenty-four hours
later, participants were tested for recovery of each fear memory. BOLD responses
during acquisition indicate similar amygdala activation to both CS+s. Consistent
with our previous published work, on day two we find extinction without
reconsolidation engages the ventromedial prefrontal cortex (vmPFC). Extinction
of the reactivated fear memory, however, fails to engage the vmPFC demonstrating
BOLD responses in this region similar to the CS-. These activation patterns
suggest the vmPFC, which is critical for extinction, is not engaged when
extinction training occurs during reconsolidation. From the test of fear
recovery on day three, we observed greater amygdala activation for the non-reactivated
CS+ relative to the reactivated CS+, consistent with the hypothesis that
safety information is incorporated into reactivated CS+'s representation
as a result of reconsolidation update. |
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