Fear without real threat can harm our mental health. Neurobiologists have found how to block this process.
Our nervous system is designed to induce fear, an essential survival mechanism. However, in the absence of tangible threats, this fear can become detrimental to our well-being. This phenomenon is particularly concerning for people who have experienced severe stress or life-and-death situations, leading to long-term and debilitating mental disorders such as post-traumatic stress disorder (PTSD).
Neurobiologists from the
University of California, San Diego have identified the biochemical changes in the brain and mapped the neural circuits that lead to experiences of widespread fear, paralyzing in contexts that are not inherently anxiety-inducing, according to their research published in the journal
Science. This discovery opens new pathways to prevent fear responses.
In their study, the team examined the brains of mice, particularly the dorsal raphe in the brainstem. They discovered that acute stress caused a change in the chemical signals of neurons, switching from "glutamate" excitatory neurotransmitters to "GABA" inhibitory ones, leading to generalized fear responses.
Delving deeper into their research, they also observed in the post-mortem brains of people who had suffered from PTSD a similar shift in neurotransmitters, from glutamate to GABA.
Research published in Science reveals the brain biochemistry and neural circuits responsible for experiences of generalized fear.
Credit: Spitzer Lab, UC San Diego A method has been developed to stop generalized fear: before exposure to acute stress, scientists injected into the dorsal raphe of mice an adeno-associated virus (AAV) that suppresses the gene responsible for the synthesis of GABA, thus preventing the acquisition of generalized fear.
Furthermore, the immediate treatment of mice with the antidepressant fluoxetine (known as Prozac) after a stressful event prevented the neurotransmitter change and the subsequent onset of generalized fear.
The researchers not only identified the location of the neurons that changed their neurotransmitter type but also demonstrated the connections of these neurons with the central amygdala and the lateral hypothalamus, regions of the brain previously linked to the generation of other fear responses.