Our brains turn intense stress into constant fear

For those struggling with the aftermath of trauma, fear lingers as a constant companion, even in stress-free situations. But why does our brain, meant to keep us safe, sometimes turn against us?

New research from the University of California, San Diego sheds light on how our brains can sometimes rewire themselves to feel fear without real threats, leading to mental conditions.

Brains response to stress

“Our results provide important insights into the mechanisms involved in fear generalization,” said Professor Nick Spitzer from UC San Diego’s Department of Neurobiology.

To understand how stress leads to fear, the scientists conducted experiments on mice. They focused on a specific part of the brain that is involved in fear.

Fear in stressed mice and humans

When we experience intense stress, something unexpected happens inside our brains. In a specific area known as the dorsal raphe, the way our brain cells (neurons) talk to each other changes dramatically.

Normally, these cells use certain chemicals, called neurotransmitters, to send messages. One of these neurotransmitters, glutamate, typically tells other brain cells to become more active. However, after intense stress, the brain starts using a different neurotransmitter called GABA instead.

GABA has the opposite effect; it tells brain cells to become less active. The shift from excitatory signals to inhibitory signals causes our brain to overreact, leading to feelings of fear or anxiety that persist long after the stressful event has passed.

The discovery isn’t just about mice. Examining the brains of individuals with post-traumatic stress disorder (PTSD), the researchers found the same glutamate-to-GABA switch. This means the change in brain chemistry that creates pervasive fear in animals is likely the same in humans.

Stopping the cycle of fear and stress

The scientists didn’t just find where the fear switch occurs – they also traced the connections of these cells to other brain areas known as the central amygdala and lateral hypothalamus. These regions are already linked to the creation of fearful reactions, adding further pieces to the puzzle.

So, can we stop this switch and prevent generalized fear? The scientists took an innovative approach using mice. They injected a special virus into the dorsal raphe region to suppress the gene responsible for making GABA.

Surprisingly, this simple procedure prevented the mice from developing generalized fear after a stressful event.

Role of antidepressants

Furthermore, the researchers tested the common antidepressant fluoxetine (Prozac) as a way to stop the transmitter switch. Remarkably, when given to mice right after they experienced stress, it prevented the onset of widespread fear.

“Now that we have a handle on the core of the mechanism by which stress-induced fear happens and the circuitry that implements this fear, interventions can be targeted and specific,” said Spitzer.

Study significance

This study offers new hope for those suffering from the debilitating effects of stress-induced fear. By understanding the specific changes within the brain, scientists can begin to design treatments that target the root of the problem rather than just the symptoms. The potential for real, lasting relief from conditions like PTSD is a tremendously exciting prospect.

This research marks a significant step forward, reminding us that even the most complex and frightening mental experiences have a biological basis. By continuing to unravel the mysteries of the brain, we move closer to a future where the lingering shadows of fear can finally be lifted.

The study is published in the journal Science.

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