Sleep can reactivate fearful memories and alleviate them, according to a new mice model research. This finding, the researchers say, could lead to the development of more effective treatments for post-traumatic stress disorder (PTSD). It was presented recently at Neuroscience 2012, the annual meeting of the Society for Neuroscience and the most extensive source of neuroscience and brain health news.

The study finds that when a frightening memory is connected with smell, this trigger – the smell – can be used to reactivate the memory during sleep without actually interrupting the sleep. The researchers – Dr. Asya Rolls of the Rappaport Faculty of Medicine at the Technion- Israel Institute of Technology in Haifa and Megha Makam of the research groups headed by Profs. H. Craig Heller and Luis de Lecea of Stanford University – found that if the reactivation is repeated, the frightening memory is strengthened; but if the re-creation is accompanied by a treatment that blocks the creation of proteins in the basolateral amygdala, the area of the brain associated with fear, the frightening memory is weakened.

PTSD is characterized by intense, highly emotional memories that are awakened by specific social and environmental triggers.

In extinction therapy, the patient repeatedly re-creates the memory in nonthreatening surroundings, such as a clinic; however, the treatment is sometimes identified with the clinic to the extent that it ceases to be effective, and the patient experiences the traumatic trigger elsewhere, such as while out on the street.

“Sleep is not linked to a specific location, and thus changes that occur in traumatic memories during sleep could weaken the fear response regardless of where the memory awakens,” Heller explains.

“This fact could provide a significant solution to the limitations of existing PTSD treatments.”

In their experiments, researchers created conditioning that paired certain smells with an electrical shock in mice while they were awake. This “control smell” was also released in the mice’s cages while they were asleep in the presence of a protein synthesis inhibitor. The activation of the conditioning smell during sleep resulted in a substantial reduction in the fear response in later tests, while the mice were awake. Most important, the decrease in the fear response was general and was not connected to a specific location.

“This is where the significant potential of the treatment of traumas during sleep actually lies. While we sleep, our brain works differently, some of our protective systems are not activated, which, in principle, allows us to access associations which might not be accessible to treatment while we are awake,” says Rolls.

“Moreover, many treatments terminate prematurely because the patient finds it difficult to deal with the repeated mention of the traumatic memories. Therefore, treatment during sleep could be an easier alternative to dealing with such memories. Of course, there is still quite a distance between these preliminary experiments and actually treating people, but it is a start.”

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