Those with added levels of RGS8 in their nervous system had shorter immobility times than those with normal levels, suggesting lower levels of depressive behavior. When given anti-depressants that work on monoamines, they had even shorter immobility times. However, when they were given drugs to stop MCHR1 from working, the immobility times remained steady, suggesting higher levels of depressive behavior.
"These mice showed a new type of depression," Saito added. "Monoamines appeared to not be involved in this depressive behavior. Instead, MCHR1 was."
Next, the team looked at the mice brains under a microscope. The mice with added levels of RGS8 didn't just act more depressed, they also had longer cilia (hair-like structures involved in cellular communication) in the regions of the brain where RGS8 concentrations are at their highest. Abnormal cilia have been linked to physical conditions, including obesity, retinal disease, and kidney disease, but this appears to be the first time it has been linked to a mood disorder.
This is significant because it could explain why antidepressants work better for some people than they do for others – and there is overwhelming evidence to show that for most people they do work. The hope is that the findings here will lead to new and more effective drugs for the people who are left behind.
If you think this could apply to you, please don't stop taking your antidepressants until you have spoken to a medical professional.