Abstract

Peptides play a key role in sleep regulation. Sleep in humans and animals is characterized by an electrophysiological component and a neuroendocrine component. In young normal human subjects the major amount of slow wave sleep (SWS), and correspondingly of electroencephalogram (EEG) delta power, occurs during the first half of the night. This electrophysiological activity is closely but not absolutely linked to the nocturnal GH peak. During this interval cortisol levels reach their nadir. This chapter presents the findings that show that GH secretagogues are capable of promoting sleep, whereas the substances investigated thus far exert different effects on the sleep EEG. It is well documented that the changes in the sleep EEG after the peptides growth hormone-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) represent CNS effects which occur independently of the changes in peripheral hormone secretion. Recent data suggests that GHRH and somatostatin exert opposite effects not only on GH release but also on the sleep EEG of the elderly. The data supports the hypothesis of a reciprocal interaction between GHRH and CRH in sleep regulation, which was first proposed by Ehlers and Kupfer. The two major conclusions that can be drawn from the reported sleep studies with GH secretagogues are that GH secretagogues are capable of promoting sleep and it appears likely that this effect is centrally mediated.

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