A team of researchers from MIT has discovered a circuit in the brains of mice that, when stimulated, can prolong the effects of therapy designed to suppress fear-related phobias. The results of the study could lead to more effective therapy aimed at people suffering from debilitating phobias such as a fear of flying, and could even aid in the treatment of more complex disorders such as post-traumatic stress disorder (PTSD).
According to the Anxiety and Depression Association of America, each year 18 percent of adults living in the US are diagnosed as having some form of fear or anxiety disorder, with 19 million of them having a specific phobia. The leading method of dealing with extreme fears, such as arachnophobia, is a treatment known as exposure therapy.
During an exposure therapy session, a patient is exposed to anxiety-provoking cues relating to their phobia in a safe environment. For example, an individual terrified of flying would be shown various images of aircraft. The repetition of this technique eventually decreases the fear reaction related to these cues, as the brain learns that nothing bad or painful will occur.
However, while the treatment is often effective in the short term, individuals are likely to have their phobias resurface through a phenomenon known as spontaneous recovery.
Advances in mankind's understanding of the human brain are gradually allowing us to discover certain connections, or neural circuits, that are activated as the brain experiences a particular emotion or state.
For some time, it has been hypothesized that such a circuit exists connecting parts of the brain that deal with fear and reward as a patient experiences exposure therapy. In order to establish whether such a circuit was in play, and whether it could be used to prolong the effects of the therapy, the researchers conditioned laboratory mice to fear a certain noise by subjecting them to a foot shock each time the audio cue sounded.
With the anxiety established, the mice were then put through exposure therapy sessions, during which the noise was sounded, and no shocks were administered. The researchers observed that, as the therapy progressed, a neural circuit was employed in the brains of the mice, connecting the basolateral amygdala (BLA) which is associated with fear memory, and the nucleus accumbens (NAc), which governs reward events.
The involvement of this connection, which the researchers dubbed the BLA-NAc circuit, suggested that the brain interprets the lack of an expected painful or unpleasant event as a kind of reward. Having established this link, the team tested the effects of actively stimulating the circuit during therapy, by either giving the mice a sugary drink as they heard the audio cue, or directly influencing the connection via flashes of light delivered through an optical wire in mice that had been genetically modified to be receptive to such stimulation.
It was found that, for mice whose neural circuit had been stimulated via the sugary drink reward, that the effects of the exposure treatment lasted 55 days longer than had been the case for mice who had gone without stimulation. Mice subjected to bursts of light from the optical cable also benefited from an increase in the amount of time that the fear reaction could be subdued.
The next step for the team from MIT is to understand how the circuit represses the fear response, and to identify whether distinct sub-circuits are active over the course of the fear learning, and subsequent counterconditioning phases of the study. Such research could one day lead to improved treatments for those suffering from debilitating phobias and PTSD.
A paper detailing the research was just published in the journal eLife.
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