Scientists from the American Salk Institute for Biological Research have uncovered a mechanism for converting sensory signals from the senses into the emotion of fear. It turned out that a special CGRP peptide helps to combine the danger signals coming from the senses and turn them into a feeling of anxiety. The protein is produced in neurons during a fright and helps to fix unpleasant memories in memory. Biologists believe that the discovery will help in the treatment of certain diseases associated with fear, in particular post-traumatic stress disorder.
Scientists from California's Salk Institute for Biological Research have found a "fear molecule". The peptide CGRP (calcitonin-gene-related peptide, encoded by the calcitonin gene) turned out to be the substance responsible for the feeling of fear during external threats. The study was published in the scientific journal Cell Reports.
This 37 amino acid neuropeptide was discovered in 1982. CGRP is now known to play a key role in the physiological mechanism of migraine pain. Drugs that inhibit the production of CGRP by neurons are used for the symptomatic treatment of attacks of this disease. In addition, CGRP is known to be involved in hematopoiesis by acting on blood stem cells and inducing them to leave the bone marrow.
The authors of the work were able to establish that CGRP also allows neurons to combine sensory threat signals from different areas of the brain into one signal, which then enters the amygdala, which is responsible for the formation of emotions, including fear.
The perception of external threats is usually associated with various external signals - visual, auditory and sensory. Science knows that different types of signals are perceived by different areas of the brain, but so far it has not been possible to understand the mechanism for combining these sensations into one alarm signal.
Previously, some studies have shown that CGRP is present in areas of the brain that send alarm signals to the amygdala. This prompted scientists to think about the role of CGRP in the formation of emotions such as fear.
“Based on data from these two studies, we hypothesized that CGRP neurons, mostly located in subregions of the thalamus and brainstem, relay threat information from multiple senses to the amygdala,” said co-author of the study, PhD student. Shiya Liu.
The team of scientists conducted a series of experiments to test the hypothesis. They tracked the activity of neurons that produce CGRP molecules in mice. At the same time, the rodents received multisensory danger signals. As a result, biologists were able to determine the path of signals after they exit the thalamus and brain stem. The authors also conducted tests to assess the level of fear in mice.
It turned out that two separate populations of CGRP neurons, one of which is located in the thalamus and the other in the brainstem, send a signal to two non-overlapping areas of the amygdala, thereby forming two separate chains.
Both populations encode information about visual images, sounds, smells and tactile sensations that pose a threat, interacting with local brain networks.
Also, scientists were able to establish that both chains are necessary for the formation of aversive memory, which makes in the future to avoid objects and situations that once caused fear.
“The brain pathway we discovered functions like a central warning system. We were encouraged by the discovery that CGRP neurons are activated by negative sensory inputs from all five senses, which are responsible for vision, hearing, taste, smell, and touch. By identifying new pathways that signal threat, a deeper understanding is emerging about the treatment of anxiety disorders,” said lead study author Song Han, senior lecturer in the Peptide Biology Laboratory at the Salk Institute for Biological Research.
According to biologists, the results obtained during experiments on mice can be applied to humans. The identified mechanism may play a role in a number of fear-related mental illnesses, such as post-traumatic stress disorder and autism spectrum disorders. Scientists do not exclude that the same drugs that are used today in the treatment of migraine symptoms to suppress the expression of CGRP can help in the treatment of such disorders.
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