Mice Might be Able to Explain Why Some Antidepressants Don't Work


Over 27 million people take antidepressants in the United States. That was doubled in the mid 1990’s and only half the people taking these antidepressants are getting relief from their depression symptoms which means half the people do get relief.

Trying to sort this out researchers called upon mice to try to explain this perplexing puzzle. “The mouse model explains why someone may not respond to antidepressants," says lead researcher Rene Hen, professor of pharmacology in the Departments of Psychiatry and Neuroscience at Columbia University. Researchers at Columbia University Medical Center in New York released a study suggesting that genetically engineered mice that had too much of one type of serotonin receptor in this region of the brain were less likely to respond to antidepressants.


“These receptors dampen the activity of these (serotonin-producing) neurons. Too much of them dampen these neurons too much," Hen said, "It puts too much brake on the system." Hen’s research team identified a receptor so they could replicate in mice what happens when antidepressants fail. Some of the genetically engineered mice were designed to have high levels of the receptor 1A, a type of receptor on nerve cells that produces serotonin.

By watching their behavior, researchers were able to determine how the mice responded to the drugs. They found that when mice take antidepressants, they act more daring but mice with high levels of certain serotonin receptors, did not act like they were on antidepressants. "There are new experimental treatments now, but deep brain stimulation is really invasive," Hen said.

"The most dramatic finding is that the mice that have high levels of receptors in these serotonin neurons do not respond to fluoxetine or Prozac," Hen said. Psychiatrist Jonathon Flint at Oxford University, who was not involved in the current research said, "The hope is that what is true for mice will be true for humans. If it is, then we have a route to improve the efficacy of antidepressants, rather than the current practice of try whatever we have and see what works."

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