New proof has put into question the long standing thinking that a lack of serotonin a chemical messenger in the brain performs a main role in depression. In the journal ACS Chemical Neuroscience, researchers have claimed that mice inadequate the capability to make serotonin in their brains did not indicate depression like symptoms.
Donald Kuhn and co-workers observed that depression creates a main public health issue. WHO reports that over 350 million individuals endure from it and it is mentioned to be the major cause of disability across the world.
In the late 1980s, the now popular antidepressant Prozac was launched. The drug functions primarily by improving the quantities of one substance in the brain that is serotonin. So researchers came to think that enhancing levels of the signaling molecule was the essential to handling depression. Depending on this concept, many other medicines to deal with the depression came into the picture. But now scientists know that 60-70% of these sufferers keep on to feel depressed, even when using the drugs. Kuhn’s group set out to research what role, if any, serotonin performed in the depression.
To do this, they developed “knockout” mice that were missing the potential to generate serotonin in their brains. The researchers ran a battery of behavioral assessments.
Curiously, the mice were compulsive and very aggressive, but did not display signs of depression like symptoms. One more amazing discovering is that when put under stress, the knockout mice acted in the similar way most of the regular mice did. In inclusion, a part of the knockout mice reacted therapeutically to antidepressant medicines in a similar way to the normal mice.
The scientists mentioned that these results may be proof that serotonin is not a main player in the depression, and that various aspects must be engaged. They came to the conclusion by indicating that these outcomes could considerably alter how the research for new anti-depressants goes forward in the long term.