Washington: A new study has recently provided a deeper insight into where in the brain does the alarm first go off when sensing danger, and what other parts of the brain are activated to express fear and remember to avoid danger in the future.
The research team looked first at the thalamus, the part of the brain known as the "switchboard." In particular, they focused on the paraventricular nucleus of the thalamus (PVT), "an area that is readily activated by both physical and psychological stressors," according to the authors.
As part of their experiment, the researchers used mild foot shocks to simulate danger. They also genetically altered mice to study the role specific parts of the circuit play in protecting the mice from "danger."
First, they confirmed that the PVT was indeed highly sensitive to threats. They then looked at the neurons in the posterior PVT (pPVT) that were communicating with the lateral division of the central amygdala (CeL), where neuroscientists say is a site of fear memories.
Through a series of experiments that suppressed communications coming from these neurons, they found that the pPVT plays an important role in conditioning the mice to fear certain situations and to remember those fears. They also demonstrated that this knowledge was "hard wired" into the neuronal synapses.
But what chemical messenger do the pPVT neurons send off to deliver this information to their cousins in the CeL? The researchers hypothesized that the messenger might be brain-derived neurotrophic factor (BDNF), a protein known to regulate synaptic functions.
To test this hypothesis, the researchers created mice without the gene to produce BDNF or without a BDNF receptor.
Both kinds of mice exhibited an impaired ability to recognize danger, even after being conditioned to do so. The researchers also tested the effect of BDNF on mice that had not been genetically altered by infusing their brains with BDNF, causing a "robust" response to danger.
The communications transmitted by BDNF produced in pPVT neurons and picked up by CeL receptors, the researchers concluded, "facilitate not only the formation of stable fear memories but also the expression of fear responses."
The study is published in Nature.