Sleep; It is a physiological need for learning, memory, and regulation of mood. At the beginning of the complaints that occur in most psychiatric disorders, changes in the quantity and quality of sleep occur. In this text; Briefly, information on the neurobiology of sleep, the neurobiology of the relationship between sleep and mood disorders, and the effect of sleep deprivation on mood disorders is presented. Sleep is primarily a function of the brain and is an active multidisciplinary process. Normal sleep has two stages: rapid eye movement sleep (NREM) and rapid eye movement sleep (REM). NREM sleep is divided into four stages according to sleep EEG patterns. NREM 1-2 is called light sleep, and NREM 3-4 is called deep sleep. Each sleep cycle takes about 90-120 minutes. The sleep cycle is repeated 3-6 times during the night.
The main areas responsible for wakefulness are the reticular formation, basal forebrain (cholinergic), locus ceruleus, dorsal raphe and posterior hypothalamus, dopaminergic A11 area, and the responsible neurotransmitters acetylcholine, norepinephrine and is serotonin. The main areas responsible for sleep are the ventrolateral preoptic area and especially the cholinergic laterodorsal tegmental nucleus and peduncular tegmental nucleus responsible for REM sleep. Related neurotransmitters are noradrenaline, serotonin, dopamine, adenosine, histamine, GABA and acetylcholine.
Sleep has a great impact on quality of life. Sleep disorders are associated with the onset, course and treatment of mental disorders such as bipolar disorder and depression, which reduce quality of life in the long term. The suprachiasmatic nucleus is the main center responsible for regulating sleep-related variables. Since this region is stimulated, melatonin secreted by the pineal gland allows sleep to begin. Sleep disturbances are common in people with depression, and sometimes sleep disturbances can begin before depressive symptoms appear. Regarding circadian variation, waking early in the morning, shortening of REM latency and shifting in intensity to the first third of the night, phase progression of body temperature rhythms, secretion of cortisol, and release of metabolites and monoamines suggest a circadian rhythm in depressed patients and Or disrupted circadian rhythms lead to depression. However, there are different models proposed for the relationship between mood disorders and sleep. In the internal coincidence model, it is suggested that there are phase differences between the suprachiasmatic nucleus and the sleep/wake cycle.
The model assumes that sleep causes depression when there is no synchronization between these two elements. The other model is the translation of one or more circadian cycles from their usual relationship with other cycles.
Whether the abnormalities of REM sleep in depression are a situational factor or a defining feature is debated.
Depression is neurobiological. model suggests that the increased REM intensity in depression is due to decreased cholinergic hypersensitivity, serotonergic, and noradrenergic sensitivity. REM sleep disorders in depression are thought to result from a complex relationship between noradrenergic, serotonergic, cholinergic, hypocretinergic and stress systems.
Some common neurotransmitters that are affected by sleep and depression and their relationships are as follows:
GABA-ergic neurons play a key role in initiating and maintaining sleep by inhibiting histaminergic and other wakefulness-producing cell populations. However, the concentration of GABA in the cerebrospinal fluid of depressed patients is low. In this case, decreased GABA-ergic activity may be associated with difficulty in falling asleep, which is a symptom of depression.
It is thought that the formation of serotonin deficiency in the central nervous system as a result of decreased serotonin production in the raphe nucleus may be responsible for the symptoms of depression.
Pons and mesencephalon Deficiency of noradrenaline released from Locus Coeruleus located in Likewise, it is known that noradrenaline is low while asleep.
Although depressed patients usually complain of insomnia, sleep deprivation therapy, which is very effective for depressed mood, is a treatment method used in depression. The rapid improvement in mood after sleep deprivation, the observation of similar effects with REM sleep deprivation or the phase progression method, the depression of circadian mechanisms that regulate sleep. points to the importance of the formation of n. Apart from the possible serotonergic, noradrenergic and dopaminergic mechanisms thought to mediate the antidepressant effect of sleep deprivation, there are several theories regarding its effects on the circadian system. Sleep deprivation practice provides improvement in mood by re-adjusting the rhythm of the S process, which is a part of the homeostatic system and contains the features of slow wave sleep in depression. Thus, slow wave sleep, whose intensity has decreased in depression, is returned to normal with a rebound effect. As it is known, REM sleep latency decreased and REM intensity increased in patients with depression. Sleep deprivation practices work by reversing these two changes. The fact that sleep deprivation and REM sleep deprivation have antidepressant properties and that some antidepressants also suppress REM sleep are the findings that draw attention to the role of REM sleep in the formation of depression.
In short; Sleep plays a role in mood disorders, both as a cause, as a symptom, and as a form of treatment. Although this inference has a much more comprehensive neurobiological basis, this is the neuroscience basis that I can convey with the available information.
Read: 0
