Neuroscientists locate cells that reprogram memories of traumatic experiences


A new study undertaken by EPFL scientists has identified how therapy can treat memories of trauma. They found that remote fear attenuation in the brain is connected to the activity of the same neurons that are also involved in storing these memories. The question the scientists have to address is whether fear attenuation involves the suppression of the original memory trace of fear by a new memory trace of safety or the rewriting of the original fear trace towards safety, but to answer that question they must first try to understand how neurons store memories in general. This study has found the importance of rewriting in treating traumatic memories, although it does not discount suppression. Professor Johannes Gräff said: "Our findings shed, for the first time, light onto the processes that underlie the successful treatment of traumatic memories".

The EPFL scientists genetically modified mice to carry a ‘reporter’ gene that produces an identifiable and measurable signal to locate neurons in the brain's dentate gyrus, which is involved in the encoding, recall, and the reduction of fear. They first identified the neurons involved in storing long-term traumatic memories by subjecting the mice to a fear-training exercise to produce long-lasting traumatic memories. Then the mice were subjected to fear-reducing training. Some of the neurons active at recalling the traumatic memories were still active when the mice no longer showed fear, and the less the mice were scared, the more cells became reactivated. This suggested that the same neurons may be involved in storing and attenuating traumatic memories.

“Neuroscientists have located the cells that help reprogram long-lasting memories of traumatic experiences towards safety, a first in neuroscience“

The scientists then reduced the excitability of the recall neurons during the exposure therapy and the mice showed poorer fear reduction. However when the excitability of other neurons in the dentate gyrus was reduced, this was not the case, which suggested the recall neurons in the dentate gyrus are required for fear attenuation. When they increased the excitability of these recall neurons during the therapeutic intervention, the mice showed improved fear reduction, which indicated that attenuating remote fear memories depends on the continued activity of the neurons they identified in the dentate gyrus.

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