An estimated one-third of people will suffer from stress or fear-related disorders at some point in their lifetime. Certain traumatic memories can stick with us and wreak havoc, causing chronic anxiety, depression, phobias and post-traumatic stress disorder (PTSD). One of the most successful trauma treatments available is a behavioral therapy called “exposure therapy.”
A method that involves re-exposing the patient to traumatic stimulus in a controlled environment in an effort to break the association of fear or anxiety. A new study out today in the journal Science examines how exposure therapy works on a cellular level and shows the effectiveness of this type of therapy relies principally on recall neurons rewriting traumatic memories.
Neuroscientist don’t yet fully understand how neurons store our memories. The mystery fuels a considerable debate in the field: Do exposure-type therapies work by suppressing a memory trace of fear and replacing it with a new memory trace of calm and safety? Or does the process involve a rewriting of the neurons that are active during traumatic recall?
Although the authors of this new study say suppression may still play a role, they were able to observe for the first time neuronal reprogramming of long-term traumatic memories.
Researchers at the Swiss Federal Institute of Technology, Lausanne (EPFL) discovered long-lasting trauma (remote fear) reduction in the brain is correlated with activation of the same neurons involved in memory storage. Looking at mouse brains, the scientists zeroed in on a group of neurons in the dentate gyrus.
The dentate gyrus is part of the hippocampus; an area critical for memory encoding, retrieval, and abatement of fear. Previous studies show the dentate gyrus plays a crucial role in generating contextual memories of fear. It also appears to generate new neurons, a process called neurogenesis.
The mice in this study were genetically modified to carry a gene that emits a signal–a fluorescent protein–following neuronal activity. The researchers used a fear-training exercise to give the mice long-lasting traumatic memories. This allowed the scientists to pinpoint a group of neurons in the dentate gyrus involved in storing and recall of long-term traumatic memories.
The mice then went to therapy (fear-extinction training) a mouse-in-a-lab approximation of exposure therapy. The scientists discovered that some of the neurons active during the recall of traumatic memories were still active when the rodents no longer showed fear. And the less the mice were afraid, the more cells were reactivated. It’s the first indication that this group of neurons in the dentate gyrus may be involved in storing memories as well as reducing the impact of traumatic memories.
The researchers put the mice through exposure therapy again, this time reducing the excitability of the recall neurons. With the recall neurons turned down, the mice showed less fear reduction (exposure therapy less effective) compared to the controls. The researchers then dampened the excitability of other neurons in the dentate gyrus, but found these other neurons didn’t seem to influence fear reduction.
Finally, the researchers excited the recall neurons during exposure therapy and saw that the mice showed a decrease in fear, demonstrating that the particular group of neurons in the dentate gyrus involved in recall are also critical for fear reduction.
“Our findings shed, for the first time, light onto the processes that underlie the successful treatment of traumatic memories,” says neuroscientist Johannes Gräff, whose lab conducted the study.
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