Researchers have discovered how stress turns into fear in the brain in post-traumatic stress disorder (PTSD), and a method to block it.
- Significant stress triggers a specific mechanism in certain neurons, like a “fear switch.”
- By blocking this mechanism, it is possible to prevent generalized fear reactions linked to a traumatic event.
- Tests on mice have demonstrated this.
The survival instinct guides our fears, but this is sometimes modified by our life experiences. For example, post-traumatic stress corresponds to anxiety and a feeling of intense fear following a traumatic event. To better understand this phenomenon and ways to counter it, researchers from UC San Diego, in the United States, devoted a study to this subject, the results of which appeared in the journal Science.
Post-traumatic stress: a change takes place in the brain
The test involved laboratory rats. The researchers analyzed their dorsal raphe, an area located in the brainstem: they discovered that acute stress induced a change in the chemical signals of neurons, going from “glutamate” excitatory, with inhibitory neurotransmitters “GABA”, this then led to widespread fear reactions. This mechanism can be compared to a “fear switch“, when activated: it is triggered.
“The benefit of understanding these processes at this level of molecular detail, what is happening and where it is happening, allows for intervention specific to the mechanism causing the associated disorders.”, notes Nick Spitzer, co-author of this work. To go further, the scientist and his team examined the post-mortem brains of humans who had suffered from post-traumatic stress syndrome. “A similar glutamate-GABA neurotransmitter change was also confirmed in their brains.”specifies communicated.
How to block fear linked to post-traumatic stress?
Next, scientists sought to understand whether it was possible to reverse this brain mechanism. In a new experiment, they injected an adeno-associated virus (AAV) to suppress the gene responsible for GABA synthesis in the dorsal raphe of mice. Then, they were subjected to acute stress. Blocking the gene prevented them from developing generalized fear. “Furthermore, when mice were treated with the antidepressant fluoxetine (under the brand name Prozac) immediately after a stressful event, transmitter switching and the subsequent onset of generalized fear were prevented.”add the specialists.
These different tests allowed the researchers to identify the location of the neurons which changed their transmitter. But it also allowed them to identify the connections of these neurons with the central amygdala and the lateral hypothalamus, regions of the brain that were previously linked to the triggering of other fear responses.
“Now that we have mastered the core mechanism by which stress-induced fear occurs and the circuits that implement that fear, interventions can be targeted and specific.“, estimates Nick Spitzer. Further research will deepen these findings.