Researchers from the University of California San Diego announced on March 14 the publication of a new study that identified the changes in brain biochemistry and mapped the neural circuitry behind our experience of generalized fear.
Nick Spitzer, a member of UC San Diego’s Department of Neurobiology and Kavli Institute for Brain and Mind, Hui-quan Li, a senior scientist at Neurocrine Biosciences, and their colleagues published their research in the journal Science on March 14.
The group claims that it has discovered the neurotransmitters “at the root of stress-induced generalized fear.”
The study was conducted on the brains of mice, specifically looking at an area in the brainstem known as the dorsal raphe.
Researchers found that “acute stress” caused a switch in the chemical signals found in the neurons, which led to a generalized fear response in the subjects.
“Our results provide important insights into the mechanisms involved in fear generalization,” said Spitzer in a press release. “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 subsequently examined the postmortem human brains of PTSD sufferers and found a similar neurotransmitter switch in those brains.
They next succeeded in stopping the production of generalized fear in the mice by injecting the dorsal raphe with something to suppress the response prior to the experience of acute stress. Likewise, the researchers also found that they could prevent the onset of generalized fear by treating the mice with an antidepressant immediately after an episode of acute stress.
“Not only did the researchers identify the location of the neurons that switched their transmitter, but they demonstrated the connections of these neurons to the central amygdala and lateral hypothalamus, brain regions that were previously linked to the generation of other fear responses,” reads the press release.
“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.
