fear switch

Scientists Found the Brain’s ‘Fear Switch’ and How To Turn it Off

In a recent breakthrough that could pave the way for novel treatments for anxiety and stress disorders, a team of neurobiologists from the University of California San Diego has uncovered a “fear switch” in the brain.   

This discovery could alter our approach to understanding and handling fear by mastering control over this neural switch, potentially offering relief to millions suffering from generalized anxiety disorders and PTSD.

“Our results provide important insights into the mechanisms involved in fear generalization,” said co-author and professor of neurobiology at UC San Diego, Dr. Nicholas Spitzer. “The benefit of understanding these processes at this level of molecular detail — what is going on and where it’s going on — allows an intervention that is specific to the mechanism that drives related disorders.”

Fear is an inherent and complex emotion that is a crucial survival mechanism. As an instinctual response to perceived threats or danger, fear triggers a flood of physiological reactions designed to prepare our bodies for either fight or flight. This automatic warning system heightens our senses, quickens our reflexes, and floods our bodies with adrenaline, enabling us to respond swiftly to potential harm. 

Despite its often intensely unpleasant sensation, fear plays a crucial role in keeping us safe, alerting us to risks, and guiding our actions to avoid or confront danger, thereby increasing our chances of survival in a precarious world.

However, when fear is irrational and out of proportion to real threats, it can escalate into severe mental health problems. Excessive fear can lead to anxiety disorders, phobias, or post-traumatic stress disorder (PTSD), significantly affecting daily life. People with acute fear disorders may struggle with everyday activities, social interactions, or even stepping outside their homes, resulting in a reduced quality of life.

Despite fear being such a prevalent emotion, the brain processes that drive this emotion have been largely unclear. To shed light on how fear works, a group of researchers from UC San Diego, led by Dr. Hui-Quan Li, aimed to uncover the brain mechanisms responsible for generating fear.

Researchers studied the brains of mice subjected to varying degrees of stress to explore the biochemistry and neural circuitry involved in generalized fear experiences. 

The lab mice used in experiments were genetically altered to produce a particular transporter for the critical neurotransmitter glutamate in their brains. Glutamate, the most common excitatory neurotransmitter in the brain, must be present in exact concentrations within specific regions for the brain to operate correctly.

The mice also had a fluorescent protein added to their brain cell nuclei. These modifications allowed researchers to effectively monitor and track changes within the brain during fear events. 

In their findings, published in the journal Science, researchers found a significant shift in neurotransmitters — from glutamate, which excites neurons, to GABA, which inhibits them — in the dorsal raphe region of the brain. This particular brain region is responsible for the regulation of anxiety and is believed to play a significant role in fear memory formation

Researchers found that when exposed to frightening situations, this change from excitatory glutamate to inhibitory GABA neurotransmitters led to sustained fear response, akin to what is observed in anxiety disorders and PTSD.

To confirm that their findings could be applied to the human brain, researchers examined the postmortem brains of individuals diagnosed with PTSD. Like the lab mice, the PTSD sufferers’ brains had a similar glutamate-to-GABA neurotransmitter “fear switch.” 

Having pinpointed a neurological mechanism responsible for generating generalized fear, researchers then explored two promising techniques to effectively turn off the brain’s “fear switch.”

In one example, researchers injected mice with an adeno-associated virus that suppresses the gene responsible for GABA. Findings showed that mice injected with the virus did not develop a “fear switch” or symptoms of generalized fear disorder. These results suggest that gene therapy, or effectively a “fear vaccine,” could potentially prevent the development of generalized fear disorders. 

In another experiment, researchers found that administering the common antidepressant fluoxetine (Prozac) immediately after a stressful event could prevent the “fear switch,” thereby averting the onset of generalized fear. This latter finding, however, comes with a caveat: timing is crucial, as the intervention loses its efficacy if delayed.

Researchers caution that their findings are not an immediate cure. However, they do provide a solid foundation for developing treatments that could one day offer relief to those plagued by fear and anxiety.

Current treatments for PTSD and anxiety disorders often fall short, partly due to a lack of specificity in addressing the underlying cause. However, this new research not only sheds light on the molecular mechanisms underpinning fear and anxiety but also identifies the neural circuitry involved. 

By pinpointing the brain’s “fear switch,” this study offers a blueprint for more effective therapies and targeted interventions in the future.

Discussing the potential impact of these findings on future mental health treatments, Dr. Spitzer said, “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.” 

Tim McMillan is a retired law enforcement executive, investigative reporter and co-founder of The Debrief. His writing typically focuses on defense, national security, the Intelligence Community and topics related to psychology. You can follow Tim on Twitter: @LtTimMcMillan.  Tim can be reached by email: tim@thedebrief.org or through encrypted email: LtTimMcMillan@protonmail.com