The circuitry in the brain that leads to anxiety first gets established in early development, according to new findings in mice by researchers from Columbia University Health Sciences and colleagues elsewhere. Their results imply that current popular drugs for adult anxiety do not necessarily treat the cause of the disorder, but may be alleviating symptoms resulting from an event that occurred long ago.

The research, published in the March 28 issue of Nature, reveals there is a window of time during the development of the mouse--between five and 21 days after birth--when the brain becomes wired to be anxious later in life. The comparable time in humans is the third trimester of pregnancy and the first two to three years of life.

The study, led by Dr. Rene Hen, associate professor of pharmacology (in psychiatry and in the Center for Neurobiology and Behavior), focused on a serotonin receptor gene. The researchers manipulated the time in development and the location in the brain that the serotonin receptor was active to understand its role in creating anxiety circuitry.

Brain neurons communicate with each other by secreting chemical messengers--neurotransmitters such as serotonin--which cross the synaptic gulf between nerve cells and bind to receptors on neighboring nerve cell membranes. Once the neurotransmitters bind to the receptors, the nerve cells become activated.

Medications that enhance the binding of serotonin to its receptor (such as the selective serotonin reuptake inhibitors, or SSRIs) work effectively to treat anxiety and depression, suggesting the receptor and the neurotransmitter play a role in regulating these emotions. Since the drugs act by increasing the amount of serotonin in the brain, scientists have presumed the disorders may be due to decreased levels of serotonin in the adult brain.
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Contact: Leslie Boen
lsb2001@columbia.edu
Columbia University Medical Center
20-May-2002

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