Sleep rhythms

Key points
- Loss of function of the SCN increases the duration of sleep, indicating that it has a wakefulness maintaining effect and tends to counteract the homeostatic drive to sleep.
- There is an important circadian pattern to the secretion of hormones, many of which are controlled by the hypothalamus [19].
- The release of ACTH is controlled both by CRH and by arginine vasopressin which also acts on osmoreceptors in the preoptic area of the hypothalamus.
- Its release is closely related to the circadian rhythm but is also slightly influenced by light exposure.
The diurnal cycling of sleep–wake rhythms maintains sleep and wakefulness in line with environmental time, but by itself is insufficient to initiate sleep (Fig. 2.8).
Loss of function of the SCN increases the duration of sleep, indicating that it has a wakefulness maintaining effect and tends to counteract the homeostatic drive to sleep. In effect it raises the threshold of the other sleep drives for initiating sleep. It does not selectively promote either NREM or REM sleep.
The SCN promotes wakefulness during the day, except between 2.00 and 4.00 pm, and particularly in the evenings shortly before the usual time of sleep onset which is when the homeostatic drive to sleep is greatest. The circadian rhythm opposes this and leads to the 'wakefulness maintenance zone' or 'forbidden zone'.
At this time just prior to the usual time of sleep it is difficult to fall asleep. The end point of this zone occurs when the homeostatic drive, together with an input from the adaptive drive, overcomes this circadian influence. The onset of secretion of melatonin by the pineal gland also inhibits the SCN activity.
The circadian drive to wakefulness is at its least before the habitual wake-up time of the subject in the morning. This helps to consolidate sleep at the end of the night when the homeostatic drive to sleep is waning. At the time of waking the circadian drive to wakefulness increases sharply and its wakefulness effect overcomes any residual homeostatic drive to sleep.
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Temperature cycle
The sleep and temperature cycles are usually closely coupled [18], although in free-running experiments the sleep cycle usually becomes around 1h longer than the temperature cycle. The temperature of the blood is sensed in the paraventricular nucleus which is close to, but separate from, the VLPO and other sleep-regulating sensors in the preoptic area of the anterior hypothalamus. Activity in these centres suppresses arousals and increases NREM sleep as well as reducing the core body temperature. Melatonin secretion facilitates sleep and also lowers the core body temperature. The peak melatonin level is seen at the nadir of the core body temperature at 3.00–5.00 am.
The paraventricular nucleus reacts to a rise in temperature by increasing heat loss through cutaneous vasodilatation and sweating. If the temperature falls, the posterior hypothalamus causes heat conservation by cutaneous vasoconstriction and increased heat production through skeletal muscle activity, including shivering, and piloerection.
The amplitude of the circadian temperature cycle is 0.5–0.75°C, although this is reduced in the elderly.
The temperature rises to a peak of 37°C at 3.00–5.00 pm and falls only slowly until around 9.00 pm. The drop in core temperature which precedes sleep is associated with an elevation of skin temperature due to cutaneous vasodilatation, possibly related to accumulation of adenosine in the basal forebrain.
Written and revised by
David Cohen, M.D.
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