Borbely [1] introduced theories of how circadian and homeostatic mechanisms influence sleep, which, subsequently, have been widely accepted. Sleep-wake cycles are controlled by circadian rhythm oscillators in the suprachiasmatic nuclei (SCN). In contrast, the homeostatic process regulates sleep need (propensity) which increases during the day and decreases during sleep depending on the amount of mainly nonrapid eye movement sleep (NREM) a person previously had [2]. The homeostatic mechanisms are able to overrule the circadian system because sleep deprivation leads to longer sleep. Adenosine is one of the main sleepinducing factors in homeostasis [3], although there are also changes in neuronal activities associated with sleep propensity [4].Over time, researchers have been increasingly able to explain various aspects of sleep, but the neurological basis of these highly complex mechanisms had remained unclear. Within this framework of circadian rhythms and homeostasis, the photic input into the SCN and the functions of these small structures responsible for circadian rhythms were strongly emphasized. However, the role of SCN, especially when it was viewed in isolation without their extensive neurological and neurochemical network, failed to explain the pathophysiology of circadian rhythm sleep disorders (CRSD).In recent years, research into the anatomic and physiological aspects of circadian rhythmicity has blossomed. Major progress has been made in understanding molecular biology of the SCN [5] and at the same time, knowledge about the roles of the thalamus and other brain structures in sleep have expanded [6][7][8][9][10][11]. Sleep is a neurological function and the process of wakefulness and sleep involves the entire central nervous system. Similarly, modulators of melatonin secretion and the effects of this indoleamine are more complex than previously thought. Melatonin receptors, clock genes, sleep deprivation, the timing of circadian rhythms, a vast number of neurochemicals, hormones, the environment, and various neurological structures and other factors are acting as a symphony to influence melatonin physiology and the sleep-wake cycle [2,5,[12][13][14].
The role of thalamus in sleepThe thalamus plays a critical role in processing, integrating, correlating, and relaying sensory and motor information [9]. Major auditory, visual, and somatosensory pathways, together with inputs from the limbic structures, the brainstem, and cerebellum have their final subcortical relays in this highly complex paired structure, which Abstract: The thalamus has a strong nonphotic influence on sleep, circadian rhythmicity, pineal melatonin production, and secretion. The opening of the sleep gate for nonrapid eye movement sleep is a thalamic function but it is assisted by melatonin which acts by promoting spindle formation. Thus, melatonin has a modulatory influence on sleep onset and maintenance. A remarkable similarity exists between spindle behavior, circadian rhythmicity, and pineal melatonin production throughout life. To...