Researchers discover how to stop the brain from feeling fear

Our nervous systems are finely tuned to detect fear, a crucial survival mechanism alerting us to potential danger. Whether it's the rustle of leaves in the night or the menacing growl of an approaching predator, fear prompts us to stay vigilant and steer clear of harm.

However, when fear arises without any real threat, it can become detrimental to our well-being. Individuals who have undergone severe or life-threatening stress may find themselves experiencing intense fear even in safe situations.

This broadening of fear responses can have serious psychological consequences, potentially leading to long-term mental health conditions such as post-traumatic stress disorder (PTSD).

Until recently, the underlying mechanisms driving this phenomenon have largely remained a mystery. However, neurobiologists from the University of California San Diego have made significant strides in unraveling these mysteries. Their findings, published in the journal Science, shed new light on the biochemical changes in the brain and the neural pathways responsible for generalized fear responses.

Former UC San Diego Assistant Project Scientist, Hui-quan Li, now a senior scientist at Neurocrine Biosciences, along with Atkinson Family Distinguished Professor Nick Spitzer and their team, delved into the research behind identifying the neurotransmitters — chemical messengers facilitating communication between neurons — underlying stress-induced generalized fear.

Their investigation focused on the dorsal raphe, a region in the brainstem, using mice as models. They discovered that acute stress triggered a shift in the chemical signals within neurons, transitioning from excitatory "glutamate" to inhibitory "GABA" neurotransmitters, ultimately leading to generalized fear responses.

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Professor Spitzer, from UC San Diego’s Department of Neurobiology and Kavli Institute for Brain and Mind, emphasized the significance of their findings, stating, "Our results provide important insights into the mechanisms involved in fear generalization.

Understanding these processes at a molecular level allows for targeted interventions to address related disorders."

Expanding on their discovery of neurotransmitter switches induced by stress, which represent a form of brain plasticity, the researchers examined postmortem human brains of PTSD sufferers. Confirming their findings, they observed a similar shift from glutamate to GABA neurotransmitters in these brains.

To combat generalized fear, the researchers devised interventions. By suppressing the gene responsible for GABA synthesis in the dorsal raphe of mice prior to stress exposure, they prevented the onset of generalized fear. Additionally, administering the antidepressant fluoxetine (Prozac) immediately after a stressful event prevented the neurotransmitter switch and subsequent fear response.

In addition to identifying the specific neurons responsible for the transmitter switch, the researchers also mapped out their connections to brain regions such as the central amygdala and lateral hypothalamus, previously implicated in fear responses.

Professor Spitzer concluded, "Now that we understand the core mechanism driving stress-induced fear and the associated circuitry, interventions can be targeted and precise."

This groundbreaking research offers hope for mitigating the debilitating effects of generalized fear induced by stress, potentially paving the way for more effective treatments for conditions like PTSD.

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