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Psycology » Psychiatry and psychotherapy » Biological bases of mental pathology » Biochemistry psychoses

  1. Etiology and pathogenesis of mental disorders
  2. Genetics of mental illness
  3. Biochemistry psychoses

Assumptions about the allocation of "special air" in the nerve endings made by W. Cullen (1776), which therefore believed that all diseases are nervous, and proposed to refer to them, the term "neurosis". Advances Neurosciences allowed now to establish that the transfer of information from one neuron to another is carried out as a result of specific binding neyrostruktur ("synapses") by allocating specific chemicals (neurotransmitters neurotransmitters). Identified and described various mediators that are released at the moment of excitation in the synapses, causing a chemical reaction occurs with protein receptors that are located on the pre - and post-synaptic membrane. Occurs as a result of either neuron excitation or inhibition of activity. After interaction with neurotransmitter receptors may be decontaminated or re-captured the presynaptic membrane (reverse neuronal uptake, reapteyk). The blockade of the receptors makes them insensitive to the action of neurotransmitter reuptake and blockade enhances its effect that leads to receptor overstimulation. In the occurrence of psychoses are particularly important catecholamines (dopamine, norepinephrine, epinephrine).


This material is synthesized from the amino acid tyrosine is a precursor of norepinephrine, is inactivated by methylation and oxidation by the enzyme monoamine oxidase (MAO). Dopaminergic neurons located in the subcortical nuclei of the midbrain (substantia nigra, the striatum) and in the hypothalamus. They send impulses to the pituitary gland, the limbic system. There comes the regulation of muscle tone, emotional state and behavior. Dopamine stimulates the central nervous system, increases motor activity, increases blood pressure (BP). Dopamine system is provided through the work of "pleasure centers" regulated affective sphere. Confirmed the role of disturbances in dopamine transmission in parkinsonism, TIR schizophrenia. Overactive dopamine system is associated with the action of hallucinogenic drugs (mescaline, which is chemically similar to dopamine). Blockade of dopamine receptors explains the main effects of the action of antipsychotics (chlorpromazine, triftazine etc.). In untreated patients with schizophrenia increased compared with the normal level of homovanillic acid (HVA), which is the product of the conversion, the inactivation of dopamine. Reducing GVK may indicate the effectiveness of treatment with neuroleptics. With the action of dopamine associated with the appearance of such productive schizophrenic symptoms as delusions, hallucinations, mania, motor excitation. Antidofaminovoe effect of chlorpromazine and other neuroleptics gives complications such as tremor, muscle stiffness, restlessness, akathisia.

Gamma-aminobutyric acid (GABA)

. It was established that not only is the GABA neurotransmitter, but also acts as a modulator of synaptic. GABA functions in many systems of the brain as a "brake substance". Those structures of the brain, which is found in the highest concentration of GABA, have both high levels of dopamine. Since GABA can cross the blood-brain barrier (BBB) ​​in the organism of patients with schizophrenia is by inhibiting GABA-transaminase can create higher concentrations of GABA in the brain. Inhibition of GABA metabolism can be achieved with glycine and hydrazine. GABA agonist is muksimol which has hallucinogenic properties. Diazepam can also be used as an agonist of GABA. Inhibition of GABA receptors in the ventral cortex increases dopamine activity in the brain and olfactory tuber causes abnormalities of behavior in animals that resemble experimental psychoses.


This material was synthesized from dopamine MAO inactivated, and then converted into vanillylmandelic acid (CMC) and 4-methoxy-4-gidroksifenilglikol (MOFEG). Norepinephrine is a hormone precursor adrenal adrenaline. The weakening of the noradrenergic activity may indicate the development of depression. Proved participation in the formation of norepinephrine emotions (anguish, fear, anxiety), the regulation of the sleep - wakefulness, implementation pain sensation.


Pronounced sedative effect in animals and severe depression in humans after large doses of reserpine suggest that such effects may be related to decreasing neuronal terminals in the brain noradrenaline and serotonin (5-hydroxy-methylamine, 5-HT, 5-HT) under the influence of reserpine. Psychopharmacological research results gave impetus to the development of the serotonin hypothesis of mechanisms of pathogenesis of depressive states. MAO inhibitors strongly affect the levels of serotonin in the brain than on the level of norepinephrine. Tricyclic antidepressants (imipramine, amitriptyline) are able to block the reuptake of serotonin in presynaptic terminals, increasing the level of serotonin in the brain. In the study of the concentration of serotonin in the brain tissue of patients with depression after the suicide of some researchers were able to determine the reduction of serotonin and its metabolites in brain tissue.


These substances are the material basis of various cell-cell interactions, acting as neurohormones, neurotransmitters, neuromodulators. The study contributes to the disclosure of their functions essentially biological processes that underlie the pathology of mental activity. Neurohormonal functions have primarily vasopressin, oxytocin, neurotensin, thyroliberin. These neuropeptides involved in such processes nervous activity such as remembering, memory consolidation, emotional reactions. Neuropeptide hormone-releasing hormone tirbotropina depression when administered to patients improves their condition, and somatostatin can deepen depression.

Endorphins and enkephalin

Endorphins and enkephalin, which include a-,? -?-Endorphins act as neuromodulators.

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