Serotonin, Sleep and Depression: A Hypothesis
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. The main difficulty faced by this hypothesis is the reason for the decrease in the level of cerebral mono...
Guardado en:
| Autor principal: | |
|---|---|
| Formato: | Capítulo de libro |
| Lenguaje: | inglés |
| Publicado: |
IntechOpen
2021
|
| Materias: | |
| Acceso en línea: | https://www.intechopen.com/chapters/75576 |
| Etiquetas: |
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
| Sumario: | 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. The main difficulty faced by this hypothesis is the reason for the decrease in the level of cerebral monoamines (primarily serotonin) during depression. 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. 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. 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. |
|---|---|
| ISBN: | 978-1-83969-199-7 |
| DOI: | 10.5772/intechopen.96525 |