This news may reveal a few startling insights concerning antidepressants. A new study from the Columbia University Medical Center claims that a surplus of one kind of serotonin receptor in the center of the brain may clarify why antidepressants are not able to alleviate symptoms of depression for around 50 percent of patients.
The study included a mouse model. This is alleged to be the first study to discover an underlying association between receptor number and antidepressant treatment. This could result in a more personalized treatment for depression, counting treatments for patients who do not react to antidepressants. Moreover, there may find more ways to recognize these patients prior to their experiencing expensive and eventually, ineffective therapies.
The study was headed by Rene Hen, PhD, professor of pharmacology in the Departments of Psychiatry and Neuroscience at Columbia University, and a study author at the New York State Psychiatric Institute.
Majority of the antidepressants, as well as the popular SSRIs, supposedly function by augmenting the quantity of serotonin made by cells named raphe neurons, which is deep in the middle of the brain. Serotonin is said to alleviate symptoms of depression when it is transmitter to different areas of brain. Dr. Hen and his colleagues found that excess serotonin receptors of the 1A type on the raphe neurons apparently sets up a pessimistic criticism loop that appears to decrease the generation of serotonin
Dr. Hen commented, “The more antidepressants try to increase serotonin production, the less serotonin the neurons actually produce, and behavior in mice does not change.”
Dr. Hen and his colleagues gauged the consequence of antidepressants with a generally used behavioral test that estimates the boldness in mice when regaining food from vivid open regions. Mice on antidepressants may typically grow to be more daring, but the drugs seemed have no such effect on mice with excess serotonin receptors.
Present genetic and imaging studies of depressed patients have apparently proposed that elevated receptor numbers of the 1A type in the raphe neurons appeared to be linked to treatment failure. So far, no direct examination of the relationship could be conducted since amount of receptors in the raphe neurons may not be changed without altering the quantity of receptors in other portions of the brain.
By means of novel methods in genetic engineering, Dr. Hen formed a strain of mouse that may be planned in such a way to generate elevated or low levels of serotonin receptors of the 1A type only in the raphe neuron. The levels existing in the mice appeared to imitate the levels in people who are apparently resistant to antidepressant treatment.
Dr. Hen mentioned, “By simply tweaking the number of receptors down, we were able to transform a non-responder into a responder.”
That approach could also succeed for patients resistant to antidepressant treatment, if drugs may be discovered to decrease the amount of receptors or hinder their activity. But first, the function of surplus serotonin receptors in people ought to be established. Dr. Hen’s lab is apparently now observing patients enlisted in clinical trials to view if receptor levels forecast reaction to antidepressants.
The study will appear in the Journal Neuron.