Researchers have located a molecule that serves as a messenger between two key areas of the brain in the genesis of fear.
Fear is a constant in the lives of people suffering from anxiety. And in times of intense stress can reach significantly limit their daily lives. A team of researchers at Cold Spring Harbor believe they have identified in mice hitherto unknown route that controls fear and can give clues to how may arise anxiety disorders. In particular they have located a molecule that serves as a messenger between two key brain areas important in the genesis of fear.
It has long been known that fear has its headquarters in a brain structure called the amygdala, but it was unclear what controls this structure. Suspicion fell on a group of neurons that form the paraventricular nucleus of the thalamus (PVT). This group of neurons is related to other brain structures involved in the regulation of motivation and mood, showing abnormal functioning in several psychiatric disorders, including anxiety, substance abuse or depression.
These structures are the amygdala itself, the nucleus accumbens, which is part of the reward system, and the anterior cingulate cortex, which plays an important role in the processing of negative emotions. In addition, the PVT is directly connected to the hypothalamus, a key structure to implement chronic stress responses and addiction.
With all these tracks researchers at Cold Spring Harbor found that the paraventricular nucleus is specifically activated when the mice learn to fear something or remember scary situations. Their findings are published in Nature. The researchers found that PVT neurons extend deep into the central amygdala, which regulates fear. And when this connection between the thalamus and amygdala PVT is interrupted, fear learning is more difficult.
Furthermore they used people with posttraumatic stress disorder (PTSD) to try to identify possible chemical messengers that could connect the two structures (PVT and amygdala). They focused on a molecule called BDNF that has been implicated in anxiety disorders. It is a nerve growth factor that plays an important role in the birth of new neurons and new connections between neurons and whose synthesis is enhanced with exercise. Patients with anxiety disorders often have mutations in this chemical messenger, BDNF, suggesting that it may have an important role in memory and learning of fear.
They saw that adding BDNF in the central amygdala of rodents triggers a fear response in mice that have not been previously exposed to a stimulus that causes fear and promotes the formation lasting memories about the feared situation. The scientists have established that regulatory circuit controls fear in mice. And the BDNF is the chemical messenger that allows the thalamus PVT exercise control over the central amygdala.
So far they have only seen in rodents, but extrapolation of the great importance of this route for the control of fear in humans remains to be seen. It is possible that things are not so simple in primates and humans in particular, and not rely simply a connection between two brain structures. This finding, in particular the role of BDNF, may explain why exercise is a good antidepressant and helps reduce anxiety and stress.