Even as the evidence for reconsolidation accumulates, the idea that the neural connections underlying our memories routinely come undone has some disturbing implications. Among the most significant is that our memories are vulnerable to inadvertent alteration. If the brain went to the trouble of storing a memory, why would it then have a mechanism that makes it so easy to erase? “It just doesn’t make sense that a cherished childhood memory should become vulnerable to erasure,” says Larry Squire, a neuroscientist at the University of California, San Diego. That vulnerability also has positive implications, however: the potential to weaken bad memories.
Brunet’s office at the Douglas Institute in Montreal, its bright-orange walls adorned with paintings and greenery, emanates a cheeriness in stark contrast to the grim nature of his research. He decided to focus his career on PTSD while still a college student in the late 1980s at L’Ecole Polytechnique in Montreal, after a gunman entered an engineering class there and killed 14 women in a shooting rampage.
New treatments for PTSD are sorely needed. A recent study showed that about 15 percent of U.S. combat troops returning from the wars in Iraq and Afghanistan show signs of the disorder. And while some effective treatments exist, they consume a lot of time and resources, and they don’t work for everyone.
Developing better therapies is easier, of course, if we know what causes the problem in the first place. One hypothesis holds that PTSD stems from a memory that is too strong, burned into the brain by hormones released in times of stress. These hormones, which surge as part of the body’s fight-or-flight response, activate cells in a part of the brain responsible for the emotional component of memory. In an evolutionary context, enhancing the storage of frightening memories makes sense: the more vividly you remember scary situations, the more likely you may be to stay away from them in the future. But in PTSD, that process appears to have gone awry, producing pathologically powerful memories that are triggered by the smallest reminder. Researchers have had some success in preventing the formation of these supermemories by dampening the stress response soon after a trauma: Brunet and his colleague Roger Pitman, a psychiatrist at Harvard Medical School, have both shown that patients given epinephrine-blocking propranolol in the emergency room are less likely to develop PTSD. “The idea was that if you could decrease the release of stress hormones following a trauma, you could influence the saliency of that memory in the future,” says Brunet.
This prevention strategy might work well in a military context, where everyone involved in a particular combat event could be given the drug, but it’s not ideal for civilians. The time window for treatment is limited, and not everyone who experiences a trauma will rush to the ER. “Even treating people four to six hours after the trauma may be too late,” says Pitman. If a treatment can’t help them, it certainly can’t help people who already have PTSD.
In 2004, Pitman–having learned of Nader’s work–had another idea: to use propranolol to try to mimic animal research on reconsolidation, much of which has focused on fear memories. Researchers studying reconsolidation had previously suggested that blocking the reconsolidation of traumatic memories in people might help make these memories less troubling. Propranolol, it turns out, acts on the part of the brain that is central to the emotional component of memory–the same area targeted in Nader’s rodent research. (Factual components of memory are stored in a different part of the brain.) By reactivating the patients’ memories, Pitman proposed, “we could reopen the window of opportunity and get a second chance to treat PTSD.”