LeDoux Lab 2011 SfN Abstracts
 
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.