It has taken 50 years, but memory research has finally put it all together to provide practical guidance to reduce forgetting of what we need to remember and promote forgetting of useless or disturbing memories.
I have blogged before about animal studies showing that bad memories can be erased. Bad memories are often created like conditioned reflexes in Pavlov’s dogs. That is, the situational context in which bad things occur act as associational cues that help cement the memory. If the cues are repeatedly present but the bad event is not, the learned associated tends to go away.
But in both animals and humans, this “extinction” as it is called is not really permanent and the bad memories can recur.
Memory researchers have recently discovered that when a memory is recalled, whether good or bad, there is a short time where it can be modified by new thought or experience, and then it is put back in storage (called “reconsolidation”). When this phenomenon was discovered, it raised the possibility that timing of extinction trials might influence effectiveness of treatments for anxiety. That is, better treatment results might occur if extinction is attempted during the vulnerable reconsolidation stage. In 2009, Joseph LeDoux and his colleagues demonstrated in rodents that timing of extinction trials did in fact influence the erasure of fear memory.
This modifiable stage provides a way to treat even really bad memories, like post-traumatic stress disorder. When a soldier, for example, recalls a bomb killing a buddy, that terrible memory is subject to modification before it is re-stored. A typical modern treatment for PTSD is to inject an anxiety-reducing drug just before the bad memory is triggered that interferes with reconsolidation of memory. This process may have to be repeated many times before the bad memory is finally gone. Now a new study from the Uppsala University in Sweden has shown that bad memories can be erased without drug.
Investigators created bad memories in human volunteers by giving them an electric shock each time a certain picture was flashed on a computer screen. They repeated this experience 16 times to establish a conditioned fear response. The next day after such training, the subjects were brought back into the test room, and the fear-of-shock memory re-triggered by showing the picture that had been associated with shock. This was repeated eight times without associated shock, as a way to produce extinction. Half of the subjects received their extinction treatments at 10 minutes later in which the fearful stimulus was repeated without any shock. The other half of the subjects were given the same extinction treatment but delayed six hours, when it was presumably too late to interfere with reconsolidation.
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.
Source:
Agren, T. et al. (2012). Disruption of reconsolidation erases a fear memory trace in the human amygdala. Science. 337 (6101): 1550-1552.
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