In my last post, I discussed, in broad terms, how fear works in the brain. Researchers are filling in the specifics all the time. Most recently, according to this, scientists have identified a specific type of brain cell as being responsible for the extinction of fear:
Importantly, it has been found that people with anxiety disorders exhibit an "extinction deficit," or a failure to "forget." However, until recently, the mechanisms of extinction have remained unknown.
As reported by Nature, Paré has found that clusters of amygdala cells, known as the intercalated (ITC) neurons, play a key role in extinction. His findings indicate that ITC cells inhibit amygdala outputs to the brain stem structures that generate fear responses. Indeed, Paré and his collaborators have shown that when ITC cells are destroyed with a targeted toxin in rats, extinction memory is impeded, mimicking the behavior seen in PTSD.
The significance of this finding derives from earlier results suggesting that PTSD reflects an extinction deficit and that the amygdala is hyperactive in this disorder. As a result, it might be possible to compensate for this abnormality and facilitate extinction with pharmacological interventions that enhance the excitability of ITC cells to inhibit amygdala outputs.
Meanwhile, researchers have found that a drug currently used to treat tuberculosis (oddly enough), D-cycloserine, affects cells in the brain's fear center, the amygdala, such that fear extinction is enhanced:
D-cycloserine, an antibiotic, is normally prescribed at a 10-fold higher dose to treat tuberculosis. The effects of the single low dose given prior to CBT exposure therapy sessions are usually imperceptible to patients and last just a few hours. Yet animal studies show that the medication interacts with a receptor in the brain's fear hub to facilitate what is known as extinction learning - learning to be less fearful...
The researchers taught rats to fear an initially neutral stimulus, a light, by repeatedly pairing it with an aversive stimulus, a mild shock. The animals then behaved fearfully when exposed to just the light. Extinguishing the fear response required repeated exposures to the light without the shock. Davis's team discovered that giving the rats just one dose of D-cycloserine just before these extinction training trials speeds up this safety learning process by making the NMDA receptor work better.
Sounds promising. Indeed, 'psychologist Barbara Rothbaum, in an editorial in the March 2008 issue of the American Journal of Psychiatry...heralded the new approach as a "paradigm shift."' We'll see; I'm sure lots of panic sufferers hope she's right. CBT therapists, too -- 'cause then they'll be able to trumpet even better outcomes.