Scientists discover ‘fear switch’ in the brain – 03/19/2024 – Science

When someone feels threatened or in a dangerous situation, the nervous system activates fear, an essential defense mechanism, which warns of the possibility of danger and puts them on alert. Sometimes, however, this state comes even without the presence of concrete threats.

Severe or life-threatening stress episodes can induce fear in situations that do not pose a real threat. Experiencing this generalized fear is psychologically damaging and, over time, can lead to mental disorders such as post-traumatic stress disorder (PTSD).

A team of neurobiologists from the University of California, in the United States, identified the changes in brain biochemistry that induce fear in the absence of threats and activated the neural circuits that cause the experience of generalized fear.

The study, published on the 14th in the journal Science, brings new ideas about how to avoid reactions to fear. Its coordinator, Hui-quan Li, conducted research at the university’s Neurocrine Biosciences pharmaceutical laboratory, identifying which neurotransmitters (chemical messengers that allow neurons in the brain to communicate with each other) are at the basis of what is understood as generalized fear induced by stress.

By studying in mice an area of ​​the brain called the dorsal raphe nucleus (DRN) in the brainstem, scientists discovered that acute stress induces a change in the chemical signals of neurons, switching from the excitatory neurotransmitters glutamate to the inhibitory Gaba, which causes widespread fear.

“The advantage of understanding these processes at this level of molecular detail, [descobrindo o que acontece e onde] allows for targeted intervention in the mechanism that drives related disorders,” explains Nick Spitzer, professor at the University of California’s School of Biological Sciences.

The team then examined post-mortem the brains of post-traumatic stress disorder patients and confirmed a similar exchange of the neurotransmitter glutamate for Gaba.

Researchers have discovered how to disrupt the production of generalized fear by injecting the dorsal raphe of mice with an adeno-associated virus (AAV) to suppress the gene responsible for Gaba synthesis before they experience acute stress. The result was positive: the experiment prevented the animals from feeling fear.

Furthermore, when mice were treated with the antidepressant fluoxetine (Prozac) immediately after a stressful event, the neurotransmitter switch and subsequent onset of generalized fear were prevented.

The team not only identified the location of the neurons that switched neurotransmitters, but also demonstrated the cells’ connections with the central amygdala and lateral hypothalamus, regions of the brain that had previously been associated with the generation of other fear responses.

The findings on how to control the fear switch are encouraging and could change the way we deal with this feeling. “Now that we know the central mechanism by which stress-induced fear occurs and the circuits that put it into practice, interventions can be selective and specific,” emphasizes Spitzer.