Monoamine improved the lives of millions who experienced depression, since when the monoamine hypothesis was been discovered by the scientists. The hypothesis of 1950s A.D. is the advanced idea for nearly all antidepressants. The hypothesis was based on the observation that a deficiency of monoamine neurotransmitters (including serotine) stimulates depression, arousing the development of treatments just like selective serotonin reuptake inhibitors (SSRIs).

But the main problem is, the drug (Monoamine) is not compatible for all. According to Neuroscientists Yumiko Saito and Yuki Kobayashi from Hiroshima University in Japan, this drug doesn’t show an effect on 30% people. He further said that they needed to find out another cause of depression. They further studied newly with mice and reached on the following conclusion.

In their previous research, it was proved while analyzing cells in vitro, Saito discovered that a protein in the brain called RGS8 helps to control the hormone receptor MCHR1, which is involved with sleep, appetite and any other emotional responses.

But new research showed that RGS8 disables MCHR1 – theoretically, it reduces depression symptoms. But it is a mystery that how this might affect depression in living animals.

To find out the right answer they started a new study in two groups with two sets of mice. One group consisting of normal animals and another group of mice genetically engineered to express higher levels of RGS8.

While testing depression on mice, both types of mice normal and RGS8 boosted were subjected to a forced swimming test, in which animals are placed into a tank of warm water so as to be unable to get out of the tank and monitored well as they swim around for a while before giving up to swim. In which to giving up to swim or immobility is considered a characteristic similar to depression.

During swimming test, RGS8 boosted mice was found less depressed because RGS8 boosted mice swum more. Furthermore, these mice were given an antidepressant drug (desipramine) that acts on monoamines, their immobility time was even further reduced.

The normal mice were given a drug SNAP94847, which stops MCHR1 from working and it reduced their time of immobility in the swimming tank. But when the RGS8 boosted mice took the same drug SNAP94847, it didn’t show any effect.

According to Saito’s explanation, it came to know that these mice showed a new type of symptoms of depression. Not monoamine but MCHR1 appeared to be involved in this depressive behavior.

The researchers found that the RGS8 boosted mice showed longer neuronal cilia in which MCHR1 is localized than normal mice did when they examined the euthanized animals’ brains under a microscope. It is beyond the ken of researchers about the relation between variation in cilia length and depression. But researchers are not ready to accept it as an accident.

The researcher team wrote down on its paper regarding their findings suggest that the increased RGS8 protein level in the CA 1 region is a possible productive factor for the extent of ciliary MCHR1. Therefore, a significant change in cilia length may be connected with the behavioral result observed in RGS8 (mice).

In the beginning, there are a lot of works to be done before knowing if the drug can be used in human or not. If it can be used in humans it will help the millions of people for whom monoamine-based drugs don’t work.

Researchers’ findings demonstrated a regulating role of RGS8 in the neurobiology in the context of depression. In conclusion, RGS8 can be used for the treatment of mood disorders as well as depression.

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