Biological Psychiatry - Vol. 2

By Hugo D'Haenen; J.A. Den Boer et al. | Go to book overview

xxIv-3
Neuroendocrinology of Sleep Disorders
Axel Steiger
INTRODUCTION
The two major methods for the investigation of human sleep are the sleep electroencephalogram (EEG) and the collection of nocturnal hormone profiles. The combination of these electrophysiological and neuroendocrinological methods in young and elderly, female and male normal control subjects; in patients with psychiatric, endocrine and sleep disorders, under baseline conditions and after administration of synthetic and endogenous central nervous system (CNS) active compounds, particularly neuropeptides and neuroactive steroids; and in related animals models has shown that, firstly, during sleep a considerable activity of various endocrine systems occurs, and, secondly, a bidirectional interaction exists between the electrophysiological and neuroendocrine components of sleep. The aim of this chapter is to summarize the current knowledge in this field, which is thought to be the prerequisite for major achievements in the therapy of sleep disorders and of psychiatric disorders as well.
SLEEP EEG AND SLEEP-ASSOCIATED HORMONE
SECRETION IN YOUNG NORMAL HUMAN ADULTS
When subjects spend a night in the sleep laboratory, their sleep EEG is analysed either visually by coding each 30-s interval of the night as a sleep stage according to standard guidelines (Rechtschaffen and Kales, 1968), resulting in a hypnogram (Figure XXIV-3.1), or by EEG spectral analysis (Steiger et al., 1993a; Trachsel et al., 1992). The hypnogram shows the cyclic occurrence of periods of non-REM sleep (NREMS) and rapid-eye-movement sleep (REMS). In young normal subjects during the first period of NREMS, the major portion of slow-wave sleep (SWS) occurs. Correspondingly, in EEG spectral analysis, the major portion of slow-wave activity (SWA) is detected. The amounts of SWS and SWA are relatively low during the second half of the night. During this interval, stage 2 sleep preponderates during NREMS. The mean value for the occurrence of the first period of REMS is about 90 min. This first REMS period is relatively short. During 8 h of night sleep, 3–6 sleep cycles are found. The duration of the REMS periods increases throughout the night. Correspondingly, the amount of REMS is higher in the second half of the night than in the first half.Near to sleep onset in a rather strict, although not absolute, association with the first period of SWS, the major peak of growth hormone (GH) secretion in 24 h is found (Quabbe et al., 1966; Steiger et al., 1987; Takahashi et al., 1968). This GH surge appears to be widely sleep dependent and is suppressed during sleep deprivation (Beck et al., 1975; Sassin et al., 1969). However, in sleep-deprived, but relaxed young men in a supine position, an unchanged nocturnal GH peak was observed (Mullington et al., 1996). During the second half of the night, GH concentrations are low. The pattern of Cortisol secretion is inverse to that of GH. After sleep onset, Cortisol reaches its nadir. Between 0200 and 0300, the first pulse of Cortisol release occurs, and it is followed by further pulses until awakening (Weitzman, 1976). Adrenocorticotrophic hormone (ACTH) is the prime stimulus of nocturnal Cortisol secretion in man. Nevertheless, the secretion of ACTH and Cortisol may dissociate (Fehm et al., 1984). In summary, during the first half of the night, SWS, SWA and GH preponderate while ACTH and Cortisol levels are low. In contrast, during the second half of the night, the amounts of REMS, ACTH and Cortisol are high while SWS and GH secretion are low. This pattern suggests
1. a reciprocal interaction of the hypothalamo-pituitary-somatotrophic (HPS) and the hypothalamo-pituitary-adrenocortical (HPA) systems (the corresponding peripheral end points are GH and Cortisol, respectively)
2. the existence of common regulators of sleep EEG and sleepassociated hormone secretion.

Indeed, there is now a good evidence that a reciprocal interaction of the key hormones of the HPS and HPA systems, GH-releasing hormone (GHRH) and corticotrophin-releasing hormone (CRH), plays a major role in sleep regulation, as indicated in more detail below.

Prolactin rises after sleep onset and reaches its peak during the second or the last third of the night. In males, testosterone rises constantly throughout the night (Weitzman, 1976). Melatonin secretion is related to the light-dark cycle and has its peak during the early morning (Zhdanova et al., 1997).

The secretion of thyroidea-stimulating hormone (TSH) and of the thyroid hormone thyroxin is related to circadian rhythm (Brabant et al., 1987; Chan et al., 1978). The minimum TSH level is found during daytime. TSH rises during the night and reaches its maximum by midnight. Then the levels decline during the early morning hours. The course of thyroxin release is inverse to that of TSH. Thyroxin levels are low during the night and increase during daytime. One study reported declining TSH levels during REMS periods (Follenius et al., 1988).

The hormone most clearly linked to the NREMS-REMS cycle is renin. Plasma renin activity oscillates throughout the night and reaches its peak during NREMS and its acrophase during REMS (Brandenberger et al., 1988) (Figure XXIV-3.6).

Most sleep-endocrine studies have been done on males. A sexual dimorphism is reported in young normal humans. Cortisol secretion is higher in females than in males. A lower amount of SWS during the second half of the night and a greater decrease in SWS and SWA from the first to the second half of the night were found in young normal women (Antonijevic et al., 1999).

Leptin, the protein product of the obese (ob) gene, is released from adipocytes in the periphery. It acts within in the hypothalamus (Elmquist et al., 1997) and reduces food intake, probably by

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