How the brain treats trauma is complex, and humans have different ways of overcoming trauma, depending on whether the trauma occurred long ago or recently. But what scientific evidence does the brain handle short-term traumatic memory and long-term traumatic memory?
EPFL scientists have identified specific areas in the mouse brain that are involved in reprogramming the traumatic experience for safety. The areas of the brain are actually different, depending on whether the trauma occurred recently or long ago. They found that enhancing the activity of a primitive region of the brain called the nucleus reuniens could promote the disappearance of long-term traumatic memory.Results will be published today Nature Neuroscience..
“Tramatic memory becomes very emotional and difficult to” erase “or extinguish. Despite this fact, surprisingly little is known about these long-term traumatic memories, “explains EPFL Chairman Nestlé Johannes Gräff. “In our study, it is the first time someone has studied the disappearance of fear at the brain circuit level for long-term traumatic memory.”
In 2018, Gräff and his team identified cells in the brain that are involved in long-term trauma reprogramming for safety, also in mice. The same cells that were activated during the trauma experience were also activated after treatment. This indicates that the traumatized cells themselves have been reprogrammed for safety and gives insight into how the brain responds to trauma at the cellular level.
However, Gräff and his team wanted to understand how traumatized brain cells were reprogrammed for safety, and whether other areas of the brain facilitated this reprogramming. It was. They found that the standard extinction pathways of recent memory are not involved in the so-called distant or long-term traumatic memory extinction.
Nucleus reuniensens promotes recovery
In the experiment, mice underwent “Pavlov’s fear conditioning” and received an electric shock from the ground. Traumatized mice express fear by freezing, but after treatment, mice regain self-confidence and normal mobility. One group of mice was treated 1 day after trauma and another group was treated 30 days later.
Scientists have determined which brain circuit was active in both groups of mice. They found that one day after trauma, the direct cortical amygdala pathway was activated, but thirty days later, the indirect pathway rooted in the nucleolus was activated.
“Interestingly, nucleoactivity peaked shortly before mice stopped expressing fear, as if nucleoactivity was anticipating the end of freezing,” Gräff continues. “When we manipulated the activity of the time-locked nucleons at these peaks, we found that they were really important for regulating fear. Therefore, increased activity resulted in less freezing of mice. When suppressed, the mice freeze more. “”
“That prediction of when the freeze will end is, in fact, perhaps the most enlightening finding of our work from a purely technical point of view.”
The results provide insights at the brain circuit level as to why traumatic memory persists and is difficult to extinguish. They shed light on the mechanisms of the brain involved in recovery from long-term traumatic memory.
Turning this recent finding into a treatment for people suffering from post-traumatic stress disorders or other long-term traumatic experiences that affect mental health remains a challenge. In collaboration with a partner agency in the Netherlands, scientists are now approving to study similar human brain mechanisms.
Researchers have found that they can indirectly regain and weaken traumatic memory.
Thalamic amygdala circuit, which underlies the extinction of remote fear memory, Nature Neuroscience (2021). DOI: 10.1038 / s41593-021-00856-y
Provided by Ecole Polytechnique Federal de Lausanne
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Overcoming long-term trauma can be facilitated through activity in the nucleus reuniens
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