Researchers have discovered that antidepressant drugs such as Prozac not only affect levels of the neurotransmitter serotonin in the brain, but also "hijack" dopamine signaling as well--causing it to launch serotonin signals. Their findings offer new insight into how Prozac and other "selective serotonin uptake inhibitors" (SSRIs) work and how they might cause problems in patients taking them.

SSRIs perform their antidepressant function by increasing the concentration of serotonin in the signaling junctions, called synapses, between neurons. This increase alleviates the deficiency of serotonin that causes depression.

As their name indicates, SSRIs prevent uptake of the serotonin after it has performed its task as a chemical messenger that enables one neuron to trigger a nerve impulse in a neighbor. SSRIs prevent this uptake by inhibiting the action of the molecular cargo carriers called transporters that recycle serotonin back to the neuronal storage sacs called vesicles.

Now, however, Fu-Ming Zhou (presently at the University of Tennessee) and colleagues at Baylor College of Medicine have revealed that SSRIs can have more complex effects on neurotransmitter traffic in the brain than just altering serotonin levels. They found that higher serotonin concentrations caused by SSRIs can "trick" transporters of another key neurotransmitter, dopamine, into retrieving serotonin into dopamine vesicles. Dopamine transporters have a low affinity for serotonin, but the higher serotonin levels result in its uptake by the dopamine transporters, found the scientists.

As a result, the normal dopamine-triggered firing from such neurons, in essence, launches two different types of neuronal ammunition, causing "cosignaling."

The researchers were led to study the role of dopamine signaling in SSRI action by previous evidence that dopamine was involved in depression and in the function of antidepressants in the brain. They studied the nature and m
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Contact: Heidi Hardman
hhardman@cell.com
1-617-397-2879
Cell Press
6-Apr-2005

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