Emory University professor Michael Davis revealed that specific brain structures can be targeted therapeutically to treat anxiety during Friday’s psychology seminar, “Role of Amygdala versus Bed Nucleus Stria Terminalis in Phasic versus Sustained Fear and Effect of a Cognitive Enhancer on Extinction” in Moore Hall.

Davis, who was the 2008 recipient of the Edward M. Scolnick Prize in Neuroscience, has found that the bed nucleus of the stria terminalis, a brain structure, is responsible for turning normal fear into anxiety via corticotrophin-releasing hormone (CRH).  The management of this fear building process holds promise for both phobia victims and patients with post-traumatic stress syndrome.

Davis’ experiments conditioned laboratory rats to associate a certain stimulus, either visual or acoustic, with fear via an electric shock in order to elicit the startle reflex. 

The goal was to locate both the hormonal messenger as well as the biological structures responsible for managing fear.  As the seminar progressed, Davis revealed that the amygdala plays a crucial role in the startle reflexes of the rats.  The amygdala is located in the inner brain and deals with the relationship between memory and emotion.  Davis discovered that two distinct structures, the central nucleus of the amygdala and the bed nucleus of the stria terminalis, have overlapping roles in the neural management of fear. 

Davis made a clear distinction between phasic fear, which comes on fast and leaves in the absence of stimulus, and anxiety, which accumulates slowly and may not have a clear cause.  What his experiments demonstrated was that the central nucleus dealt with predictable, conditioned fear, but cannot respond to the sustained stress of fear.  In situations of prolonged danger, such as war, corticotrophin-releasing hormone (CRH) is released and binds to receptors that are specific to the bed nucleus to create symptoms typically associated with anxiety.

Davis quoted the nightly torment of a Vietnam veteran, who was catapulted back into the death-strewn battlefields of his military service by something as benign as a thunderclap, and went on to describe chemicals that could potentially remove the pathway of anxiety. 

For example, a new drug called D-Cycloserine quickens the extinction of fear by acting as an agonist to the glutamate receptors of the amygdala, allowing more calcium to enter.  Davis also made it implicitly clear that any change made to the amygdala pathway was not an eraser of memory, but rather “inhibitory learning.” 

Using D-Cycloserine, agoraphobic patients in psychotherapy classes reduced their average number of sessions from eight to two.  

Davis has opened the door for understanding not only the cognitive nature of anxiety, but also its possible eradication through