Three important neurotransmitters belonging to the same amino group are called monoamines, norepinephrine (norepinephrine), dopamine and serotonin. Like acetylcholine, norepinephrine was discovered long ago, because it is also located outside the brain. This is the main chemical that regulates the physical changes that accompany emotional recovery. It is also found in the brain and plays the role of a neurotransmitter responsible for the feeling of hunger, wakefulness and waking up from sleep. Serotonin is found in all parts of the brain and plays an important role in regulating sleep. Dopamine is the main neurotransmitter in areas of the brain that provide consistent movements of body parts. This discovery gave rise to the hypothesis that dopamine deficiency can be the main cause of Parkinson’s disease, which affects mainly older people and is characterized by progressive movement inconsistency, hardening of muscles and trembling in the body. In accordance with this hypothesis, new approaches to the treatment of

Parkinson’s disease began to be applied, including the use of the drug L-DOPA, the “initial substance” of dopamine. L-DOPA was prescribed to patients to restore the level of dopamine in the tissues, and gave amazing results. Acceptance of dopamine itself is ineffective, since it cannot get into the brain along with blood. The brain is protected from toxic substances by the blood filtration system or the blood barrier of the brain (encephalogen barrier), which also detains dopamine. But L-Dofa overcomes this barrier and, getting into the brain, turns into dopamine. The use of L-Dov in the treatment of Parkinson’s disease is a vivid example of the value of scientific studies of neurotransmitters. Although L-Dova does not eliminate the disease at all (the loss of dopaminergic neurons continues, and even this drug cannot completely fill it), it prolongs the life of people with Parkinson’s disease, who would have died many years earlier without it.

In addition to these functions, monoamines are closely related to mood and emotional disorders. The discovery of substances affecting monoamines has revolutionized psychiatry. There is strong evidence that severe clinical cases of depression are associated with biological disorders. According to the latest theories, clinical depression occurs due to changes in the level of monoamines, especially norepinephrine and serotonin. This is also confirmed by the fact that drugs destroying monoamines cause depression. As we have said, reserpine causes leakage in the vesicles of nerve endings and the subsequent destruction of neurotransmitters, as a result of which there is a shortage of monoamines in the body. Drugs used in the treatment of depression significantly increase the production of norepinephrine and serotonin.

Monoamines, and especially dopamine, also constitute the biochemical basis for the occurrence of another serious mental illness, schizophrenia. When it happens, there is an almost complete loss of connection with reality, manifested in deceptions of feelings, hallucinations, disturbed emotional reactions and falling out of public relations. It is proved that these symptoms are caused by increased activity of monoamines. First, all drugs used to treat schizophrenia block monoamines. There is a very close relationship between the strength of the therapeutic effect of the drug and its ability to block dopamine receptors. In addition, compounds incapable of this, as a rule, do not relieve the symptoms of schizophrenia, even if they possess all the other properties inherent in effective drugs. Another interesting piece of evidence: stimulant drugs such as cocaine and amphetamines increase dopaminergic brain activity. Although small or moderate doses of these stimulants improve mood, overdosing often leads to paranoid disorders and loss of connection with reality, which almost exactly repeats the symptoms of schizophrenia. When the effect of the drug diminishes and dopaminergic activity returns to normal, these symptoms disappear. This again indicates a connection between increased dopaminergic activity and schizophrenia.

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