Faster-acting antidepressants may finally be within reach

IMAGE: These are CCK neurons (red) within the mouse dentate gyrus. The cells produce p11 (green), a protein the researchers showed is necessary for SSRI action.
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Credit: Laboratory of Molecular and Cellular Neuroscience at The Rockefeller University/Neuron

Some activity patterns in the brain can be dangerous, producing persistent dark moods that drain people’s motivation, pleasure, and hope. For the past thirty years, pills like Prozac or Zoloft–collectively known as selective serotonin reuptake inhibitors, or SSRIs–have offered millions of Americans a way to shed the heavy cloak of depression and attain more wholesome states of mind.

These medications were designed to increase nerve cells’ access to serotonin, a chemical that helps the brain regulate certain emotions. Yet researchers still don’t know precisely how the drugs work to adjust errant brain chemistry, or how to make them work better.

Now, a team of Rockefeller scientists has for the first time described how SSRIs initiate their action by targeting a particular type of nerve cell. Their findings, published last week in Neuron, may provide a path to new antidepressants that would not only be safer to use than existing ones, but that would also act more quickly.

Lucian Medrihan, a research associate in the lab of neuroscientist and Nobel laureate Paul Greengard who led the study, explains that while existing SSRIs can produce moderate effects within hours or even minutes, most people don’t really begin to feel better until they’ve been on the drugs for a significant amount of time–a major drawback when it comes to treating clinical depression. The drugs may also cause a wide range of uncomfortable side effects, including nausea, dizziness, weight gain, and sexual dysfunction.

Finding the cells that matter

The basic idea behind SSRIs is relatively simple. When a neuron releases serotonin to signal another cell, it normally reabsorbs excess amounts of the…

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