[CLASSICAL MUSIC] NARRATOR: Memories are useful for our survival. They allow us to remember the location of food sources, avoid dangerous situations, and form relationships. However, memories can be harmful to us as well. They can cause us a lot of emotional stress, and they can even initiate disorders such as post-traumatic stress disorder, or PTSD, panic disorder, depression, and phobias. 

If we can interfere with these harmful memories after they are stored, we can treat patients with these disorders much more easily. Fortunately, recent research on memory shows that every time we recall a memory, it becomes labile, or malleable, once again. At this malleable state, we can change, update, or erase parts of memories. But how do we know all this? So this film is made to explain exactly that. 

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When a memory is acquired, it is first temporarily stored in our short-term memory. Then, the memory undergoes a protein synthesis or, simply, a stabilization process that strengthens the memory and stores it in long-term memory. This process is called consolidation. 

According to traditional consolidation theory, researchers thought that memories undergo this stabilization operation once, after acquisition, and that's it. You cannot affect a memory after this stabilization process is complete, they thought. However, in recent experiments, neuroscientists found results that conflicted with this theory. 

In 2000, Nader, Shafe, and LeDoux designed an experiment with rats to understand whether we can change memories after they're consolidated. They decided to, first, create an aversive memory in rats and wait for it to be consolidated. Next, remind the rats of this memory the following day. And once the memory is recalled, try to disrupt the memory with a drug. And finally, test the rats to see if they still remember the original aversive memory. 

So they started their experiments by creating aversive memories in rats. They trained these rats by presenting them with a tone [MUSICAL TONE] followed by a shock to their foot, which is a stimulus that they find unpleasant. As a result of this training, rats learned to associate the tone with the food shock and to expect the food shock whenever they heard the tone. This training is a commonly used behavioral paradigm known as aversive conditioning or fear conditioning. 

So to test if they could erase this aversive memory after it had been consolidated, they came into the lab on day two and presented the tone [MUSICAL TONE] once without the food shock to remind them of the aversive memory. In other words, they reactivated the aversive memory. 

Shortly after the reactivation of the memory, the researchers injected either a protein synthesis blocker, anisomycin, or simply the regular cerebrospinal fluid, ACSF, into the amygdala, the emotion center of the brain. They predicted that if the stabilization process or the protein synthesis was done once, that is only after acquisition, the protein synthesis blocker would not affect the aversive memory. 

But if the stabilization needed to be repeated whenever the memory was reactivated, anisomycin could disrupt this process, impair, or maybe even delete the aversive memory. The next day, they tested their rats to see whether they still remembered to expect the food shock when they heard the tone. 

They quantified their freezing response [MUSICAL TONE] as a sign of aversion and compared the responses of rats that received anisomycin to their control group rats, meaning rats that had received the regular brain fluid ACSF instead of the drug. 

When they looked at their results, they saw that rats that had received the drug anisomycin displayed less freezing in response to the tone, suggesting that their memory of the aversive stimulus was impaired. So it seems like memories become susceptible to changes when they are recalled. And if their stabilization is disturbed, they can be impaired. 

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You might be asking, but how about humans? Similar fear conditioning experiments were conducted with humans, and researchers were able to impair aversive memories in human subjects as well. So human memories can be changed after initial acquisition, too. Taken together, these experiments have shown that the old model of memory processing does not give us the whole picture. 

The new model suggests that when a memory is acquired, it is first stored in short-term memory temporarily. Then, it undergoes the consolidation process to be stored in long-term memory. Afterwards, whenever we recall this memory, we reactivate it and render it malleable. 

When reactivated, a memory needs to be reconsolidated through a similar protein synthesis process. If we interrupt the memory during this process, we can update it and store it in its new form. And this protein synthesis process in the new model is called reconsolidation. 

So where do we go from here? As you can imagine, interruption of reconsolidation could be a very useful strategy for therapy, if it is used in the right way. In fact, recent studies reported promising results in impairing problematic memories in cases of PTSD, phobia, and addiction. For now, we need to conduct more experiments to confirm these promising results, understand the reconsolidation process better, and explore therapeutic implications of these findings. 

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