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Depression is a mental disorder that affects many people around the world. A study led by Hiroshima University (HU), showed how protein- RGS8 plays a role in depression behaviors. This study builds upon previous work in which research team found that RGS8 controls a hormone receptor-MCHR1. Parts of the brain involved with movement and mood regulation show signs of RGS8 expression.
MCHR1, when active, regulates sleep, feeding, and mood responses. The researchers found that RGS8 inactivates MCHR1 in cultured cells. Thus, the idea is that less RGS8 means increased depressed behavior. However, this effect had never been examined in a living being. Researchers studied depression in mice in two scopes: at the behavioral level, and at the immunohistological level. First, the mice did a swim test, which is a common behavioral analysis method to assess depressive behaviors in animals.
Researchers measure the time each mouse was active, then subtract it from the total test time, leaving researchers with an immobility time period. Mice with more RGS8 in their nervous system recorded shorter immobility times than those with a normal amount of RGS8. When given an antidepressant drug that acts on monoamines, though, the RGS8 mice had even shorter immobility times. However, when the mice were given a drug that stops MCHR1 from working, immobility time did not change.
The research team examined the size of cilia sprouting from cells in a region of the hippocampus called the CA1, where RGS8 concentration was highest. Cilia are TV antennae-like organelles involved in cellular communication. The team found that RGS8 mice not only had less depressed behavior than those without extra RGS8, but they also had longer cilia. That is, mice that took the drug that stopped MCHR1 from working had longer cilia.
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