It should be noted that not only specialists showed interest in the action of mediators . At one time, not only in popular literature, but also in magazines and newspapers far from medicine , articles about these mysterious “substances of the soul” were often “skipped “, with the help of which, as it were, one could achieve complete balance and even happiness.
In the 70 years of the twentieth century was developed the theory of occurrence of depression, in the framework of which serotonin is seen as a biologically active substance, responsible for mood enhancement that provides control over the level of aggressiveness, sudden impulses arising in including sexual, regulation of appetite, cycle “sleep- wakefulness ”, sensitivity to pain and suicidal tendencies.
Since then, many experiments have been carried out. The results of many of them were controversial and contradicted each other. However, scientists have also come to agreement on a number of important issues. Thus, it is assumed that some clinical similarity between the phenomena of anxiety and depression does indeed imply the same subtle changes in the tissues of the brain; it is no coincidence that these disorders often occur together in mixed anxiety-depressive disorder.
Anxiety appears to be associated with increased activity in serotonin- sensitive brain systems . When prolonged anxiety these systems are overly active and gradually “tired”: in which can decrease the level of not only serotonin, but in the future in other systems and levels of norepinephrine, that ultimately leads to the development of depression. By the way, a number of new generation antidepressants are effective precisely due to their complex effect on the content of both mediators in synaptic clefts.
In patients with an increased level of anxiety and irritability, the endings of the brain nerve cells that are sensitive to serotonin function at the minimum acceptable level. In normal, non- traumatic conditions, this deficiency is practically (or almost) not manifested. But once stress arises , the ability to control anxiety and aggressiveness drops dramatically. In unfavorable situations, people with signs of an anxiety-depressive state experience feelings of tension and discomfort. At the same time, the activity of the endocrine organs, namely the hypothalamus-pituitary-adrenal system, is activated , and the release of the stress hormone cortisol increases .
The suppression of the tissues of the nervous system that are sensitive to serotonin under the influence of cortisol occurs faster and deeper than in a person with normal, that is, a high level of activity of nerve cells that are sensitive to serotonin. This explains the loss of the patient’s ability to manage anxiety and aggressiveness. In turn, increased anxiety and aggressiveness affect the general mood, exacerbating the further development of depression.
Another theory of the development of depression focuses on dysregulation in brain systems that are sensitive to norepinephrine. The results of a number of studies have suggested that the development of depression, especially depression, manifested without apparent external causes, stress and other adverse situations, melancholy and apathy is due to a decrease in the content of so-called catecholamines in certain brain structures, one of which is norepinephrine .
It is noted that some drugs – antidepressants block special endings of nerve cells – adrenergic receptors , affecting the release of norepinephrine. This substance becomes more, which is required for treatment.
As is often the case in science, competing theories ultimately unite organically, thereby defining a new, deeper ̆ view of the problem.
So, according to a later view, there are two ways of developing depression. One is associated with norepinephrine depletion and involves treatment with certain antidepressants, formerly desipramine or imipramine, today mitrazapine and duloxitine . The other is associated with serotonin deficiency and, accordingly, focuses on therapy with drugs such as selective serotonin reuptake blockers – sertvaline , fluoxetine, etc. In addition, it is assumed that antidepressants have a therapeutic effect by facilitating the transmission of both norepinephrine and serotonin.
Recent research in brain physiology shows that the norepinephrine- sensitive system has a significant effect on the serotonin- responsive system . The nerve cells of the former partly control the rate at which serotonin is released from the cells of the other system.
Another biologically active substance of the brain, which is considered a precursor of norepinephrine, can play a significant role in the mechanisms of the development of depression. This is dopamine , which takes part in the regulation of the motor sphere, the formation of certain behavioral reactions and has a psychostimulating effect. This view is supported by the positive results of the use of the drug L-DOPA, which is a chemical precursor of dopamine and, in turn, norepinephrine.
In addition, it has been observed that taking medications that lower dopamine levels can lead to depression. To These include, in particular, drugs Rauwolfia ( raunatin ).
A decrease in dopamine levels is also observed in some neurological and somatic diseases accompanied by depression. In an example, can cause Parkinson’s disease.
The development of depression can also be aggravated by low levels of endorphins in the brain . These biologically active substances, which have the properties of both transmitters of nerve impulses and hormones, are responsible for a person’s susceptibility to pain. Indeed, patients with depression tolerate pain worse due to a lack of endorphins, their pain perception threshold is lowered.
In depression, a decrease in the content of gamma-aminobutyric acid in certain brain systems was found . This substance, released into the blood, lowers the level of anxiety. It also takes part in regulating the flow of nerve impulses by blocking the release of other neurotransmitters, in particular dopamine and norepinephrine. As a result, disorganization occurs in the interaction of nerve cells, which process the information entering the brain and integrate motor and regulatory activity.