To measure the amount of fear evoked by later presentations of the picture, investigators objectively measured the amount of fear, using a skin conductance test that measured essentially how sweaty the palms were. Signs of fear were absent in the group given extinction trials at 10 minutes when reconsolidation was still in progress. But signs of fear persisted in the six-hour group.
To pursue questions about what was happening in the brain, investigators used brain imaging, and particularly noticed activity changes in the amygdala, a structure deep within the brain that is hyperactive in the presence of fear memories. On the third day, all subjects were brought back to the lab and brain scans run when the fearful image was shown. In those subjects in the six-hour group, activity in the amygdala predicted whether signs of fear (skin conductance) would return. No such prediction occurred in the 10-min group. In other words, people who lost their fear memory, as indicated by skin sweating, also lost the signs of the memory in the amygdala. Similar effects were seen in the network of other brain areas linked to the amygdala in the processing of fear memories.
None of this should have been surprising. Back in the 1960s, I and many others conducted studies in animals that showed memory of a learning event depended on what happened shortly after the learning. We knew that this short window of time was vulnerable to other mental events that could prevent memory consolidation. Implications for education were obvious: multi-tasking, for example, introduces mental events that interfere with memory consolidation. But one wonders why it took science 50 years to apply what we knew about consolidation to the treatment of anxiety disorders. The key was the recent discovery that recall of a memory puts it back in the vulnerable position of having to be reconsolidated.
Agren, T. et al. (2012). Disruption of reconsolidation erases a fear memory trace in the human amygdala. Science. 337 (6101): 1550-1552.