The serotonin transporter gene may affect neural circuits connecting the amygdala and the cingulate and cause depression.

People with anxiety disorders or depression complain not so much about the emotion itself as its unceasing nature, says Daniel Weinberger of the National Institute of Mental Health. Now he and his colleagues may have found why their experience is continuous, according to work published in the June issue of Nature Neuroscience. Scientists know that the serotonin transporter gene, which encodes a key protein for neurotransmission in the brain, comes in a long form and a short form. People who have the short form are susceptible to developing depression or anxiety, though the gene does not actually cause it. To find out how the short form affects emotional health, Weinberger’s team looked at 94 healthy individuals, some who have each form. Using brain imaging techniques, they found that two regions involved in emotional responses, the amygdala and the cingulate, were smaller in people with the short gene. Also, the neural circuits connecting the amygdala and the cingulate were weaker in people with the short form than in those with the long one. That is important, says Weinberger, because the amygdala controls a person’s response to fearful situations, evaluating whether they should react or not, and then the cingulate vets the amygdala’s response. If a fear signal put out by the amygdala is not justified, the cingulate turns it off. But in people with the short form of the gene, the cingulate is not able to perform this editing function as effectively, so it is as if the amygdala is going off all the time. “If you can’t shut off fear, it is much worse than just feeling it for the first time,” Weinberger says. The new evidence suggests that this phenomenon happens in people with the short gene, which would explain why they are more prone to depression and anxiety.

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