Fear is a hard-wired human emotion that, when functioning efficiently, produces a lifesaving reaction to life’s mishaps. While fear is helpful in dealing with catastrophy, it often induces debilitating inaction, ranging from “exam blank” to psychiatric disorders such as generalized and social anxiety.
Anxiety disorders affect over two million Canadians each year, inhibiting their ability to function in the world. In the eyes of a person suffering from social anxiety, a routine trip to the grocery store can seem threatening due to an irrational fear of being ridiculed by others. Treatments, such as systematic desensitization behavioral therapy, exist for treating anxiety disorders such as this. In this form of therapy, patients work with a psychiatrist to become exposed little by little to their anxiety triggers. The hope is that eventually they will be able to manage their fear while completely exposed. However, fear-renewal can prevent patients from transferring their therapeutic improvements from the context of their therapist’s office. Fear-renewal occurs when a patient who initially learns to overcome their anxiety in one context suddenly encounters their past fear in a different context, reviving the old fear response once again.
Improving the understanding of fear-renewal is critical to strengthening therapies aimed at anxiety disorders. Fortunately, an article recently published in the journal Nature provides a new biological perspective.
Lead researcher Dr. Cyril Herry and his team from the Friedrich Miescher Institute for Biomedical Research in Switzerland set out to determine which, if any, neuronal circuits in the brain instigate fear-renewal. To investigate this question, the team employed an army of mice, each one fitted with electrodes in their basal amygdala. This almond-shaped portion of the brain was chosen because previous research suggested it was important in the mediation of both fear and fear-renewal.
The team conditioned fear into the mice via both loud noises and mild shocks, and then desensitized them to such treatments. The researchers were able to produce fear-renewal responses by placing the mice in new contexts and reintroducing the old fear-inducing noises and shocks. With help from the implanted electrodes and subsequent behavioral and brain analyses, the researchers pinpointed two groups of nuclei in the amygdala responsible for modulating fear-renewal responses. When these nuclei fire, their neuronal circuits connected to other parts of the brain instigate renewal of fear.
“Our data show that the [basal amygdala] contains distinct populations of neurons for which activity is oppositely correlated with high and low fear behaviour,” the researchers wrote. “Our findings are consistent with the idea that in mammals, as in invertebrates, switches between appropriate behavioural states can be driven by discrete neuronal circuits. It may be a general principle of the functional micro-architecture of the nervous system in diverse species, that circuits mediating switches between distinct behavioural states are located in close anatomical proximity thereby allowing for local interactions.”
With the mapping of the neuronal circuits responsible for fear-renewal complete, the researchers can determine how to best modulate them in order to prevent context-dependent fears from reoccurring. In the future, a drug may be able to tip the balance of activity between the neuronal circuits in order to help prevent fear-renewal and treat anxiety disorders.
