Scientists Discovered and Deactivated a Brain Fear Switch

The sensation of hairs standing on end, the cold sensation in the stomach, the rapid heartbeat triggered by a sudden movement in the shadows—these experiences evoke fear. Fear, while capable of causing distress and discomfort, can also be oddly exhilarating. However, it serves a crucial purpose as an instinctual reaction to danger, potentially enhancing our chances of survival in threatening situations.

However, there are instances where fear doesn’t align appropriately with the circumstances. In conditions such as anxiety disorders and stress disorders, the fear response can become exaggerated relative to the individual’s situation or surroundings, significantly affecting mental well-being and overall quality of life.

Research Insights and Mitigation Strategies

To gain a deeper understanding of fear and its mechanisms, a research team led by neurobiologist Hui-Quan Li from the University of California San Diego has analyzed alterations in brain chemistry and neural signaling in mice subjected to intense frights. More importantly, they’ve discovered methods to mitigate it.

“Our findings offer crucial insights into the mechanisms underlying fear generalization,” explains neurobiologist Nicholas Spitzer from UC San Diego. “Understanding these processes at such a molecular level—identifying what’s happening and where—enables interventions targeted specifically at the mechanisms underlying related disorders.”

The research involved mice that were genetically engineered to express a specific transporter of the neurotransmitter glutamate in the brain, along with a fluorescent protein within their brain cell nuclei, enabling the team to monitor brain changes.

The mice received electric shocks of varying intensity under controlled circumstances. When reintroduced to the same environment two weeks later, the mice displayed a tendency to freeze in response to fear.

Exaggerated Behavior in Mice and Neurological Insights

Mice subjected to intense shocks displayed freezing behavior even in unfamiliar environments, indicating an exaggerated response. Analysis of their brains revealed the underlying mechanism triggering this heightened fear reaction.

The researchers focused on the dorsal raphe, a region in the mammalian brainstem responsible for mood and anxiety regulation, as well as supplying serotonin to the forebrain. Importantly, the dorsal raphe is heavily involved in fear learning processes.

The researchers discovered that experiencing a severe fright altered neuronal activity by shifting the neurotransmission mechanism from glutamate, which stimulates neurons, to GABA, which inhibits neuronal activity. This switch seemed to prolong the fear response, which would typically diminish or cease, resulting in symptoms consistent with generalized fear or anxiety disorders.

Neurotransmitter Shifts in Deceased Subjects

Examining the brains of deceased individuals who had experienced PTSD revealed a similar switch from glutamate to GABA neurotransmission, providing a foundation for exploring ways to mitigate the fear response.

One approach involved injecting mice with an adeno-associated virus designed to inhibit the gene responsible for GABA production. When these mice were exposed to fear stimuli, they did not exhibit the symptoms of generalized fear disorder observed in untreated mice.

However, implementing this preventive measure would necessitate prior awareness of potential stressors that could lead to the disorder.

Nevertheless, the researchers discovered a way to alleviate the impacts of fear post-incident. Administering the common antidepressant fluoxetine immediately after experiencing a fright prevented the neurotransmitter switch and consequent development of generalized fear.

However, the administration had to be prompt. Giving the drug after the neurotransmitter switch had already taken place and the fear response had manifested was ineffective. Researchers suggest this might elucidate why antidepressants frequently fail to produce desired outcomes in PTSD patients.

While it’s not a definitive cure yet, it marks a hopeful beginning toward potential effective treatments.

“Now that we comprehend the fundamental mechanism underlying stress-induced fear and the neural circuits involved,” Spitzer explains, “interventions can be tailored to target specific aspects.”

Read the original article on: Science Alert

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