• Can someone explain this like I’m not a neurochemist?

  • 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.

    CCK neurons (red) within the mouse dentate gyrus. The cells produce p11 (green), a protein the researchers showed is necessary for SSRI action.

    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.


  • Ill be happier when they can decide what a pill will do before prescribing it.

    The pill popping bingo of finding the right med and dose to ease symptoms without crazy side effects boggles my mind.

  • Interesting. Is this maybe similar to how CCK is related to infant soothing?

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