Neuroscientists at Switzerland's EPFL have for the first time homed in directly on the specific cluster of neurons in the brain responsible for reprogramming long-term memories of traumatic experiences. The research brings neuroscience closer to answering the long-held question of whether therapy simply works to suppress fear-based memories or whether it actually helps rewrite those memories.

The groundbreaking research set out to examine what mechanism the brain uses to attenuate fear-based memories, and whether this attenuation process occurs in the same place as the traumatic memory is recalled. The study used genetically modified mice that are engineered with a fluorescent protein that allows scientists to directly observe neuronal activity.

The mice were initially subjected to a fear-based exercise to implant long-term traumatic memories. It was found that a specific cluster of neurons located in the dentate gyrus were primarily responsible for recalling those traumatic memories.

The mice were then subjected to what is called exposure therapy. This is the most effective therapy used in humans today to help break traumatic associations usually involved in cases of post-traumatic stress disorder (PTSD), anxiety, and a whole host of phobias. Exposure therapy involves gently exposing a patient to the trigger of their trauma, and has been found to effectively reduce, over time, the patient's fear response.

A big question in the field of neuroscience has been whether this exposure therapy produces new neural pathways that suppress the original traumatic imprint or whether it actually works to rewrite those recall processes.

After subjecting the mice to a fear-reducing process modeled on human exposure therapy, the researchers examined activity in the animal's brains. Unexpectedly, the same cluster of neurons identified as initially recalling the fear-based memories were still active, despite the mice displaying less fear behavior. Fascinatingly, the more these specific cells were activated, the less fear the mice displayed.

When these recall neurons were artificially subdued, the mice displayed poor fear reduction tendencies, but when they were excited while in process of undergoing the exposure therapy, a significant fear reduction was identified. Importantly, it was also found that altering other areas of the dentate gyrus showed no effect in fear attenuation, suggesting the researchers had, in fact, successfully homed in on the specific cluster of neurons in the brain responsible for traumatic recall.

The exciting conclusion from this compelling study is that this small, specific cluster of neurons in the dentate gyrus is both responsible for the recall of traumatic memories and responsible for the attenuation of those memories. The researchers suggest that although this doesn't entirely exclude the hypothesis that traumatic memories are suppressed through exposure therapy, it does show that the neuronal pathways that can trigger the recall of trauma can potentially be rewritten through therapy.

The research was published in the journal Science.

Source: EPFL

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