![]() ![]() And due to the receptor diversity, ligands of serotonin receptors can effect both activating and inhibitory processes on the brain and behavior in general. ![]() Only the upper olive complex (part of the auditory system) and the optic chiasm are devoid of serotonin afferents. ![]() Due to the abundant “treelike” branching, several hundred thousands of serotonergic neurons of the brain stem innervate tens of billions of other neurons in the human brain: practically all the nerve cells of the neocortex, hippocampus, striatum, and hypothalamus, other parts of the brain as well as motor neurons of the spinal cord. Secondly, the extraordinary variety of types (at least 7) and subtypes (at least 14 some researchers even count more than 20) of their receptors, among which there are both membrane depolarizing (subtypes 5-HT2A-C, 5-HT3, 5-HT6, 5-HT7) and hyperpolarizing it (5-HT1A,B). The serotonergic system has two characteristics: first, the unusually numerous ramifications of its axons (up to a million bifurcations of a single axon). The total number of such cells in human brain is relatively small - about one hundred thousand. As is known, the largest accumulation of serotonergic neurons in the brain is observed in the dorsal raphe nuclei (DRN) and the pons varolii (zones B6 and B7 according to Dahlström & Fuxe ). The history of its study goes back about 70 years, nevertheless, serotonin remains one of the most mysterious neurotransmitters. Serotonin (5-HT) is one of the oldest and most important mediators in the central nervous system, participating in a wide range of behavioral, physiological and pathological processes. As a possible way to of non-drug treatment of depression, not deprivation, but fragmentation of this phase of sleep is suggested, that is much easier for patients to tolerate. In this review, a third cause is proposed, which can explain a number of cases of «spontaneous» onset of depressive symptoms in apparently healthy people, as well as links the hypotheses of “monoamine deficiency” and “disturbances in circadian rhythms.” It is assumed that the formation of endogenous depression is due to a combination of two factors: a reduced “basal” level of cerebral serotonin and excessively long pre-morning periods of REM sleep, during which the release of cerebral monoamines stops altogether. It is assumed either increased activity of the MAO enzyme, which metabolizes serotonin, or a mutation with the loss of function of the gene of the Tph-2 enzyme, which synthesizes serotonin, as possible causes. The main difficulty faced by this hypothesis is the reason for the decrease in the level of cerebral monoamines (primarily serotonin) during depression. For most cases of endogenous depression (major depression), the hypothesis of monoamine deficiency, despite a number of limitations it faces, is still considered the most acceptable explanation. ![]()
0 Comments
Leave a Reply. |