How the brain's 'central alarm system' gathers threats and turns them into fear
How the brain's 'central alarm system' gathers threats and turns them into fear
ISLAMABAD, (Online) - Fear is a natural emotion in humans and animals that can help detect and respond to real or perceived danger.
When a person perceives a possible threat, biochemical reactions occur to prepare the body and mind to respond — known as the fight, flight, or freeze response.
A 2016 research review discusses that this fear response is processed in a brain region called the amygdala. When faced with a possible threat, the brain receives information from the sensory systemTrusted Source through sight, sound, smell, and touch. Then, this information activates parts of the amygdala to initiate the behavioral reactions required to deal with the threat.
Yet the brain pathways responsible for gathering threatening information from the body’s sensory system and initiating the fear response are not fully understood, but new research offers some clues.
A recent studyTrusted Source from the Salk Institute for Biological Studies in La Jolla, California, may have uncovered one of those pathways.
In the study, scientists discovered populations of a molecule called calcitonin gene-related peptide (CGRP) that allows neurons to transmit threatening cues between separate areas of the brain, then relay that information to the amygdala.
The pathway between sensing danger and the fear response
To conduct the research, scientists used single-cell calcium imaging to record the CGRP neuron activity of mice exposed to threat cues that stimulated multiple senses.
Using differently colored fluorescent proteins, they were then able to track the pathways of signals leaving the thalamusTrusted Source — a brain region responsible for relaying sensory information — and brainstem. After identifying these pathways, researchers conducted behavioral tests on the mice to assess fear and memory.
When analyzing the data, the scientists discovered that two separate groups of CGRP neurons in the brainstem and the thalamus relay signals to the nonoverlapping area of the amygdala — forming two pathways. In addition, the CGRP neuron populations also translate threatening sensory input and communicate it with other brain networks.
The scientists also found that both pathways are involved in forming unpleasant memories, which may help an individual avoid the same threat in the future.
Study authors suggest that identifying these pathways may offer insights into treating fear-based mental health conditions.
In addition, they hope to examine if they play a role in multisensory stimuli processing issues, including migraine, autism spectrum disorder (ASD), and post-traumatic stress disorder (PTSD).
According to a press release, co-first author Sukjae Joshua Kang said, “drugs that block CGRP have been used to treat migraine, so I’m hoping that our study can be an anchor to use this kind of drug in relieving threat memories in PTSD, or sensory hypersensitivity in autism, too.”
The link between overactive neuron pathways and fear-based mental health conditions
Elizabeth Fedrick, PhD, LPC and owner of Evolve Counseling and Behavioral Health Services in Phoenix, Arizona, told Medical News Today:
“While a certain amount of fear and anxiety are normal, an over-exposure to fearful or stressful events has the potential to result in causing the fear pathways to become “hyperactive.” When the fear pathways become hyperactive, this often results in the development of [..] fear-based mental health disorders.”
MNT also spoke with Sung Han, PhD, senior author of the study and assistant professor at the Salk Institute, about factors that may cause these pathways to become overactive in some people but not others.
“Genetic causes, like mutation or polymorphism of the genes specifically involved in this neuronal pathway, may intrinsically alter the signal transmission of this pathway,” Dr. Han said.
“Alternatively, acquired traumatic experiences may also alter the plasticity of this pathway. Both cases may cause hyperactivity or lower the activation threshold of these neurons, thereby making them easily activated. These people may perceive otherwise normal sensory stimuli as aversive.”
– Dr. Sung Han, senior author of the study and assistant professor at the Salk Institute Investigating the relationship between neuron pathways, the amygdala, and autism
Previous research has found that autistic children with anxiety had larger right amygdala brain volumes than non-autistic children. MNT asked Dr. Han if these findings could correlate to the pathways discovered in the Salk Institute study. He said:
“We do not know since we have not investigated the correlative relationship between the enlarged amygdala and the hyperactivated central alarm pathway that we claim. We can measure the size of the amygdala in mice before and after activating this pathway artificially to test these causalities.”
Although future research may test these relationships, Dr. Han told MNT:
“Our immediate plan is to compare the activity of this central alarm system in normal and autism mouse models to examine whether mutation of autism candidate gene contributes to the hyper excitation of the central alarm network we identified.”
