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Antidepressants ineffective in some people because of high numbers of serotonin receptors? US researchers have discovered a possible reason for the ineffectiveness of antidepressants in a region of the brain in mice. They found many serotonin receptors there that could probably inhibit the effects of an artificial increase in serotonin levels through medication.
The researchers working with Jesse Richardson-Jones from Columbia University in New York published the results in the current issue of the American journal “Neuron” (Volume 65 Issue 1).
In the past, it has long been assumed that people treated with medication who responded less well to antidepressants might have many of the serotonin receptors mentioned above. But there was always a discrepancy between the assumption and the verifiability.
Richardson-Jones and his colleagues were now able to make a definitive statement because they genetically engineered the mice in such a way that they were able to specifically increase or decrease the number of said receptors. They were able to determine that the test animals with an above-average number of autoreceptors hardly or at all responded to the drugs of the group of selective serotonin reuptake inhibitors (SSRIs). If the researchers reduced the number of receptors, they could register an effect.
The background to the high media attention of the results is, among other things, the discussion that has been smoldering for years about the role that ONE substance (in this case serotonin) and of course above all the administration and effect of a medication play in depression.
Serotonin and Depression- The Monoamine Theory In the event of depression, mood, sleep behavior and emotional processes are often affected. These are all functions that are strongly influenced by serotonin. Therefore, from a biochemical point of view it seems conclusive that the serotonin in the organism of the person concerned has something to do with it.
This view probably emerged in the 1950s, when a high blood pressure (reserpine) was thought to cause depression and it was subsequently claimed that it would cause a deficiency in said serotonin and another hormone (noradrenaline). Since both belong to the group of the so-called monoamines, this thesis was called the "monoamine theory".
The drugs of the group of selective serotonin reuptake inhibitors (SSRIs), for example with the active ingredient paroxetine, increase the serotonin concentration in the synaptic gap - this is the space between the end of a nerve cell and the next cell to which the stimulus is to be transmitted (mostly muscle or other nerve cells) - because they have a strong inhibitory effect on the reuptake of serotonin, which ultimately prevents the deactivation of the neurotransmitter.
There are also other treatment models: The active ingredient tianeptine, which is contained in the drug Stablon® from the French pharmaceutical company Les Laboratories Serviers is a so-called serotonin reuptake amplifier (SSRE). It does exactly the opposite of the SSRIs at the synaptic cleft. It speeds up the reuptake of serotonin. And it is also said to be antidepressant and anxiolytic with fewer side effects than SSRI. In Germany, the drug for the treatment of depressive disorders is not approved and is not available.
Other theories of the generation and treatment of depression As mentioned earlier, the neurotransmitter noradrenaline is also suspected to be linked to depression and that the current agents may also influence noradrenaline and thus depression. The effects of dopamine are also discussed in connection with depression.
Not only from a biochemical point of view, it seems very difficult to make clear statements in the case of such complex mechanisms of action as those of neurotransmitters without recognizing and (in treatment) observing relationships. Because just as a neurotransmitter has several influencing mechanisms and locations in our organism, this also applies to a drug with its active ingredients.
Recently, researchers from Dr. James E. Gangwisch of Columbia University Medical Center in New York on results that support the thesis that too little sleep, especially in adolescents, could lead to depression and thoughts of suicide.
Washington State University researchers in Richland, Washington, according to Foodconsumer, reported that women who took vitamin D also had an impact on depression. As early as 2002, the psychologist Prof. Irving Kirsch from the University of Hull in England stated that placebos achieve an average of 82% the effects of antidepressants and in his latest book "The emperor's new drugs: Exploding the antidepressant myth" even believes that the Thesis that depression is caused by a chemical imbalance in the head is simply wrong.
Richardson-Jones and colleagues now want to demonstrate these mechanisms in humans. Even before starting drug treatment, you should be able to test for the presence of many autoreceptors and, if necessary, block them with inhibitors. But an important point is: Personal fate and the psychotherapeutic approach are left out in a purely biochemical perspective. (Thorsten Fischer, naturopath osteopath 15.01.2010)
1. Book by Irving Kirsch:
Kirsch, Irving (2009). The Emperor’s New Drugs: Exploding the Antidepressant Myth. London: The Bodley Head