Neurochemical processes in depression

At the moment about 30 mediators have been found. Dopamine , norepinephrine, and serotonin are involved in the pathogenesis of depression . Norepinephrine is active in the limbic system and hypothalamus. He is responsible for the reaction to stress, memory processes, physiological drives, emotions. Serotonin is responsible for the human emotional sphere. The connections between neurons are plastic and depend on personality traits, stress, hereditary factors, past experience. The transfer of impulses from one neuron to another is carried out using mediators. When transmitting an impulse ,    transition of an electrical impulse into a chemical signal. Mediators accumulating in the axon are released from it and through the synapse are supplied to another neuron. Mediators have a tropism for different types of receptors. After the transfer of information from one neuron to another neurotransmitter is released from the receptor, it is returned into the synapse. There it is incorporated into the transmitting neuron, or is destroyed by monoamine oxidase . The pathogenesis of depression is associated with a decrease in the sensitivity or density of the postsynaptic serotonergic and noradrenergic systems. According to the theory of S.N. Mosolova        the leading theory is the monoamine theory. The theory postulates that depression develops in due to a lack of dopamine, norepinephrine, serotonin.  

 In the late 70s of the twentieth century, the serotonergic theory of the origin of depression was developed . Based on this theory, serotonin has been considered as a neurotransmitter responsible for improving mood. He was also responsible for aggressiveness, sleep-wake cycle, appetite.

 In the 1950s, the catecholamine theory of depression was formulated . The concentration of norepinephrine in the cell is under the control of presynaptic adrenergic receptors . Stimulating these receptors inhibits the release of norepinephrine and decreases neurotransmission .     

The blockade of these receptors by antidepressants leads to an increase in the release of norepinephrine. Studies of the reticular formation of the brain have shown that antidepressants have a psychostimulant effect. Medicines in this group improve wakefulness, enhance perception, memory, thinking, and increase concentration. According to this theory, endogenous depression is caused by a decrease in the concentration of catecholamines, in particular norepinephrine, in different parts of the brain. The activity of the noradrenergic system is assessed by the concentration in the urine of MOFEG (3-methoxy-4-hydroxyphenylethylene glycol).   

 In patients with depression with low MOFEG positive therapeutic effect was observed by desipramine and imipramine .    

Dopamine deficiency may play a role in the development of depression.

Dopamine takes part in the regulation of the motor sphere, is responsible for the formation of certain behavior, and has a psychostimulating effect. This theory is supported by the ability of L-DOPA to promote increased activity. 

Endorphins are to neuropeptides having a dual function -mediatora and hormone. Endorphins are responsible for a person’s sensitivity to pain, which is why their reduced amount in dysthymia leads to pain intolerance in people with depression.  

Various neurochemical processes leading to depression are targeted by drugs. 

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