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Health and medicine

Discovery could lead to new treatments for depression

WASHINGTON - Scientists have discovered a protein that seems to play a crucial role in developing depression, a finding that could lead to new treatments for the illness - and a fundamental understanding of why it strikes.

Although problems with the mood-regulating brain chemical serotonin have long been linked to depression, scientists don't know what causes the disease that afflicts 18-million Americans.

The protein, named p11, appears to regulate how brain cells respond to serotonin, researchers from Rockefeller University and Sweden's Karolinska Institute report in the journal Science.

Most depression medications used today are members of the Prozac family that work by making more serotonin available to brain cells. They stem from a theory that depression patients might not have enough serotonin, a neurotransmitter, or chemical that carries signals between nerve cells.

Then scientists discovered the serotonin connection was more complicated, dependent on how well the neurotransmitter binds to receptors, or docking ports, on cell surfaces. Fourteen different serotonin receptors have been discovered.

The research focuses on one of those, dubbed the "1B" receptor, that seems to play a key role in depression.

Researchers found the p11 protein increases the numbers of these receptors on the surfaces of cells, mobilizing them so they're available for serotonin to do its job.

That led to experiments, using mice as well as brain tissue saved from the autopsies of depressed patients, that found:

Depressed people have substantially lower levels of p11 in their brain tissue than the non-depressed. So did a breed of mice that exhibit depression symptoms.

Then the mice were given two older antidepressants - one known as a tricyclic, the other an MAO inhibitor - and electric shock therapy. Each treatment increased the amount of p11 in mice brains, even though each therapy is known to work in different ways.

So the researchers bred mice that had no p11-producing gene. They acted depressed, and had fewer 1B receptors and less serotonin. Mice genetically altered to produce extra p11 acted in the opposite way - no depressionlike behavior, and their brain cells carried extra serotonin-signaling receptors.

[Last modified January 6, 2006, 01:05:09]