Functional Magnetic Resonance Imaging (fMRI) scans revealed that subjects who inherited one or two copies of the short variant of the human serotonin transporter gene experienced greater activation of the amygdala when shown the pictures than those with two copies of the long variant of the gene. The gene's effect on the amygdala's response to emotional stimuli may help shape a dimension of temperament, suggest Drs. Ahmad Hariri and Daniel Weinberger, NIMH, and colleagues, in the July 19, 2002 Science.

"How biologically reactive we are to a signal of danger, which is partly heritable, can place us at risk for an anxiety disorder or it may be an adaptive, positive attribute, such as increased vigilance, depending on the circumstances," explained Weinberger. "Anxiety is a complex experience not caused by any one gene or environmental factor. By showing how a variation in a gene exerts its influence on the brain's center for fear processing, this finding may lend credence to earlier reports linking the short gene variant to slightly higher levels of anxiety. It provides potential insight into one factor that contributes to the way people experience emotion."

Each of us inherits two copies of the transporter gene for the chemical messenger serotonin , one from each parent. It codes for the protein in neurons that recycles secreted serotonin from the synapse. Serotonin reuptake inhibitors (SSRIs), the most widely prescribed medications for anxiety and depression, act by blocking the transporter. The two common genetic variations occur in a region of the gene that acts like a dimmer switch, controlling the level of the gene's turning on and off. This leads to transporter proteins that function somewhat differently. The short
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Contact: Jules Asher
NIMHpress@nih.gov
301-443-4536
NIH/National Institute of Mental Health
18-Jul-2002