New evidence challenges the conventional wisdom that the brain chemical serotonin is responsible for maintaining mood balance, and that a deficit of serotonin leads to depression.
The causes of depression have long been in dispute, with scientists acknowledging that there is generally no single cause of this common mental illness diagnosis. Many researchers believe it is related to the neurochemistry of the brain, and specific neurotransmitters, such as serotonin.
But the latest research suggests that the serotonin theory of the cause of depression is simplistic and likely false.
In a study, scientists report that mice lacking the ability to make serotonin in their brains did not show depression-like symptoms. Mice are often studied in this manner, because they have simpler biological symptoms than humans, while also being capable of exhibiting symptoms similar to depression in humans.
Donald Kuhn, Ph.D., and colleagues at Wayne State University School of Medicine set out to study what role, if any, serotonin played in the development of depression.
To do this, they developed “knockout” mice that had been genetically altered to prevent the production of serotonin in their brains. Then, scientists ran a battery of behavioral tests on the special mice.
Interestingly, researchers found the mice to be compulsive and extremely aggressive, but didn’t show signs of depression-like symptoms.
Another surprising finding is that when put under stress, the knockout mice behaved in the same way most of the normal mice did. And some of the knockout mice responded therapeutically to antidepressant medications in a similar manner to the normal mice.
These findings further suggest that serotonin is not a major player in the condition, and different factors must be involved, according to the researchers.
The study was a small animal study. Because it was an animal study, it would need to be replicated in humans to determine if its findings hold up.
If the study is replicated, a new approach for the development of antidepressants may be called for.
The study is published in the journal ACS Chemical Neuroscience.
Source: American Chemical Society