Early Wiring of Brain’s “Fear” Centers Could Produce Long-term Consequences
New research shows that our brains may be hardwired to become sensitive to stressful environments at an early age and, if overstimulated, this may contribute to anxiety disorders and even psychotic syndromes later in life.
The study, which appears in the journal Brain Structure and Function, focuses on two structures deep in the brain. The central nucleus of the amygdala (Ce) is thought to be involved in responses to immediate threats and stimulus, such as becoming startled or freezing in reaction to a loud noise. The bed nucleus of the stria terminalis (BST) is thought to be involved in regulating a person’s state of vigilance, such as determining whether or not an environment or a situation poses a potential threat. Animal and human studies show that when the BST is activated by a threatening situation, we tend to slow down, become quieter, and stress hormones spike.
While Ce and BST reside in different parts of the brain, the two areas are hardwired to each other by axonal tracts – basically, bundles of long distance axon fibers that enable the separate regions to communicate with each other. However, until now it has not been clear when these connections form or the way in which they interact with each other.
In the study published today, a team of researchers led by Julie Fudge, M.D., with the Department of Neuroscience observed that these connections are made at a very early stage of development in non-human primates. They also found that the direction of the connection is essentially a one way street. The Ce – or immediate fear signaling center – conveys information to the BST, the structure that mediates general threat sensing or anxiety states. This arrangement suggests that repeated activation of the Ce by immediately fearful or traumatic events may shape long-term anxiety states in the BST.
These findings have important implications because they suggest that immediate fear-inducing events may not only have lasting input on the BST, but may do so during a period when these circuits are actually being connected. More specifically, because the connections between these two regions are formed at a critical period in the brain’s development, traumatic experiences early in life could become embedded in the brain and result in long-term consequences, which could be manifested in something as relatively benign as an “anxious temperament” or contribute to more serious conditions like mood disorders and depression.
While the researchers acknowledge that there is a great deal of individual variation in terms threat processing and response, the findings could help researchers better identify vulnerable individuals –including specific age groups – who may be at higher risk for anxiety disorders if confronted with a barrage of fear-inducing experiences. The goal of the research is to help guide discussions about how resilience and vulnerability of this core fear circuitry develops in children, and whether it can be altered by repeated or extended traumatic experiences early in life with consequences for later mental health.
Mark Michaud |