Researchers from Hiroshima University (HU), Japan, have proposed a new explanation for the biological mechanism behind depression, according to a study published in the journal Neuroscience.
Currently, most treatments for depression are based on one hypothesis of how the mental disorder arises. This explanation, known as the monoamine hypothesis, states that depleted levels of the chemicals serotonin, norepinephrine and/or dopamine in the brain—which are all different types of monoamines—result in depressive symptoms.
The vast majority of antidepressant drugs are designed based on this idea. Their purpose is to normalize the levels of these chemicals. However, around 30% of people experience no beneficial effects from these treatments, according to neuroscientists Yumiko Saito and Yuki Kobayashi from HU’s Graduate School of Integrated Arts and Sciences.
"Obviously, we need a new drug," Saito said in a statement. "We need another explanation for what could cause depression."
The new study highlights the role of a protein known as RGS8 in influencing depressive symptoms. The team’s previous research led them to formulate the idea that less RGS8 increased depressive behaviors, however, this effect had never been examined in a living organism before.
To find out whether their hypothesis was correct or not, the team conducted experiments on two groups of mice, one of which had been genetically engineered so that they had more RGS8 in their nervous system (the other group consisted of normal mice).
In a test which is commonly used to assess depressive behaviors in animals, the two groups of rodents were forced to swim in water while the researchers measured the amount of time that they were active or immobile.
They found that the mice with more RGS8 in their bodies were immobile for a shorter amount of time than the normal mice, indicating that they were less depressed.
"These mice showed a new type of depression," Saito said. "Monoamines appeared not to be involved in this depressive behavior."
In light of their findings, the researchers argue that RGS8 should be the focus of future studies. Understanding the role of this protein in causing depression could lead to the development of new antidepressant drugs that may benefit those who are unaffected by monoamine-focused treatments.
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