Fear is a necessary emotion , but in its proper measure: it is as bad to have little (which leads to reckless behaviors) as too much: then we face anxiety disorders.
The scientists knew that the learning and memory of this feeling came from a brain region called the central amygdala , but they did not know what neural mechanism activated it.
Now neuroscientists at Cold Spring Harbor Laboratory have refined further and, after conducting experiments on mice, point to a group of neurons called the paraventricular nucleus of the thalamus (PVT). Apparently, this area of the gray mass is extremely sensitive to stress situations.
As explained in the journal Nature , the nerve cells of the PVT are deeply rooted in the central amygdala ; When scientists disconnected this link, laboratory animals stopped learning to react with fear to stimuli. It is, therefore, an ideal target for developing drugs against anxiety disorders.
The key to this connection , as the study authors found when analyzing data from people suffering from post-traumatic stress disorder, lies in a molecule called BDNF, a chemical messenger associated with anxiety disorders and which plays an important role in the birth and connection of neurons. . By increasing the levels of BDNF in the central amygdala of the mice, they displayed more fearful behavior and created long-term memories of the situations that had caused them distress.
