Experiments on mice have questioned the link between depression and a lack of serotonin.
Writer JK Rowling once experienced a severe episode of clinical depression. Fortunately for her and for all of humanity, she managed not only to overcome the disease, but also to describe it in the Harry Potter books vividly and terribly – in the form of dementors, creatures that feed on human happiness. When a Dementor is around, it seems as if there will never be any joy again. This is how a depressed person feels.
According to WHO estimates, more than 350 million people suffer from depression in the world, and this figure is probably underestimated at times – after all, many do not even suspect that they are sick, but attribute their condition to weakness of will or worldly troubles. Meanwhile, depression is considered the main cause of disability and even suicide. Therefore, the world needs effective drugs, and in order to develop them, it is necessary to understand the chemical mechanism of depression.
For several decades, there has been a consensus in the scientific community on this topic: it is believed that the problem is in the lack of a hormone and a neurotransmitter (that is, a substance through which neurons receive and transmit an electrical impulse) serotonin. It is with serotonin that the principle of action of the most popular drugs, antidepressants, is associated.
But here’s the problem: they help only 30-40% of patients. The low effectiveness of such drugs led biologists from the American city of Detroit to the idea to once again check the original premise: is it really all about serotonin? The experiments were conducted by a team of specialists from the John D. Dingell Medical Center at the US Department of Veterans Affairs and the School of Medicine at Wayne University, by the way, founded in 1868. The study was led* by Professor Donald M. Kuhn and an article about the work was published in the ACS Chemical Neuroscience journal of the American Chemical Society.
For experiments, a mouse was bred that lacks a gene that determines the ability of receptors to capture serotonin, that is, a functionally “serotonin-free” mouse. It would seem that such an animal should be incredibly sad and depressed, but no – these mice did not show any symptoms of depression. Moreover, under conditions of stress (unfortunate animals were hung by the tail and thrown into the water), they fought for life in the same way as their unmodified counterparts. True, they still differed from normal mice in increased aggression. Finally, the most incredible thing: some of the experimental mice, despite the inability to “assimilate” serotonin, responded to antidepressant therapy in the same way as mice from the control group.
According to the researchers themselves, their result calls into question the traditional ideas about the role of serotonin in the neurophysiology of depression; most likely, it is more complicated and is associated with the action of some additional factors. Biologists believe that experiments on “serotonin-free” mice should be continued, because in the future they can lead to a breakthrough in the understanding of depression – and, therefore, in its treatment.
*ACS Chemical Neuroscience, August 2014.