Neurotransmitter theories of the onset of depression

Research on depression and the mechanism of action of antidepressants has led to several neurotransmitter hypotheses for the onset of depression. Of these, the catecholamine theory was subsequently most widespread. It is assumed that the cause of depression is a lack of norepinephrine in the central nervous system.        

The catecholamine hypothesis has been applied to manic-depressed psychosis. For a long time, it was believed that manic symptoms are a consequence of an excess of catecholamines, in particular norepinephrine, as opposed to depression associated with their deficiency. In recent years scientists interested in the role of dopamine in the development of affective and manic episodes. Dopamine is responsible for the development of many symptoms of mania, delusions in the structure of a manic episode, increased activity, etc.           

Another theory concerns the pathology of serotonergic processes. Serotonergic mechanisms are involved in the realization of the symptoms of impulsivity, anxiety, depression, and suicidality.  

Some scientists associate the development of mania with a lack of acetylcholine. According to this hypothesis, cholinergic structures under certain conditions have a pathological effect on monoamine metabolism and cause affective disorders. Gamma-aminobutyric acid (GABA) plays a regulatory role in the activity of other systems. GABA may facilitate the release of norepinephrine in the limbic structures of the brain.     

Neurotransmitters act on surface synaptic receptors and trigger cascades of intracellular reactions. The agents of these intracellular reactions are usually called secondary mediators, or mediators. Among the secondary (intracellular) mediators, cyclic AMP and phosphatidylinositol have been studied in detail . The clinical effect of lithium is associated with the effect on the phosphatidylinositol cascade of intracellular reactions. Lithium ions in therapeutic concentrations inhibit the metabolism of phosphatidylinositol in nerve cell cultures and in experimental animals. A clinical study revealed a decrease in the concentration of phosphatidylinositol in platelets during MDP. In another study detected anomaly phosphoinositol accumulation in neutrophils. Phosphatidylinositol metabolism in cell cultures obtained from persons with bipolar disorder is impaired. The concentration of phosphomonoesterase during mania is higher than during remission.               

Other biological factors (neuroanatomical, neuroendocrinological) correlate with the diagnosis of bipolar disorder. But to date, there are no biological markers that would confirm this diagnosis.       

Very often, scientists turn to the hypothalamic-pituitary-thyroid axis. Thyroid function depends on the emotional background, in the same time, the emotional background in many respects depends on the state of the thyroid gland. According to studies receiving thyroid hormone has a positive effect on for some affective disorders. The beneficial effect of hormone therapy is revealed even in patients with normal thyroid function. Some researchers suggest that the brain can be in a state of functional hypothyroidism with a normal concentration of hormones in the blood. Functional hypothyroidism is the result of certain disorders in the synthesis, transfer or metabolism of thyroxine. In affective disorders, a violation of the conversion of thyroxine is revealed. Other scientists report the presence in the brain of an excessive amount of thyroxine-dependent agents. The appointment of large doses of thyroxine promotes the binding and elimination of these substances. 

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