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Neurobiologists from the University of California San Diego have discovered a “fear switch” in the brain and have figured out how to turn it off.
While fear is often important in keeping us safe from harm, making us aware of dangerous situations and surroundings, it can also be debilitating if it manifests itself as a generalized anxiety disorder, phobias, or post-traumatic stress disorder.
“Overgeneralization of fear to harmless situations is a core feature of anxiety disorders resulting from acute stress, yet the mechanisms by which fear becomes generalized are poorly understood,” the scientists wrote in their study, published in the journal Science.
Some people can find themselves in a near constant state of “fight or flight,” living a poor quality of life as a result. This study aims to help those who suffer from this disability.
“Our results provide important insights into the mechanisms involved in fear generalization,” said Dr. Nicholas Spitzer, co-author of this new study and professor of neurobiology at UC San Diego. “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.”
The researchers explained that “generalized fear in mice results from a transmitter switch from glutamate to γ-aminobutyric acid (GABA) in serotonergic neurons of the lateral wings of the dorsal raphe. Similar change in transmitter identity was found in the postmortem brains of individuals with posttraumatic stress disorder (PTSD).
“Overriding the transmitter switch in mice prevented the acquisition of generalized fear. Corticosterone release and activation of glucocorticoid receptors mediated the switch, and prompt antidepressant treatment blocked the cotransmitter switch and generalized fear.
“Our results provide important insight into the mechanisms involved in fear generalization.”
This led the researchers to the conclusion that blocking this “switch” prevented fear generalization, “suggesting that this mechanism could be targeted for preventing some of the deleterious consequences of acute stress.”
“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 Dr. Spitzer.