As neurophysiological investigations of sleep cycle control have provided an increasingly detailed picture of events at the cellular level, the concept that the sleep cycle is generated by the interaction of multiple, anatomically distributed sets of neurons has gradually replaced the hypothesis that sleep is generated by a single, highly localized neuronal oscillator.Cell groups that discharge during rapid-eye-movement (REM) sleep (REM-on) and neurons that slow or cease firing during REM sleep (REM-off) have long been thought to comprise at least two neurochemically distinct populations. The fact that putatively cholinoceptive and/or cholinergic (REM-on) and putatively aminergic (REM-off) cell populations discharge reciprocally over the sleep cycle suggests a causal interdependence.In some brain stem areas these cell groups are not anatomically segregated and may instead be neurochemically mixed (interpenetrated). This finding raises important theoretical and practical issues not anticipated in the original reciprocal-interaction model. The electrophysiological evidence concerning the REM-on and REM-off cell groups suggests a gradient of sleep-dependent membrane excitability changes that may be a function of the connectivity strength within an anatomically distributed neuronal network. The connectivity strength may be influenced by the degree of neurochemical interpenetration between the REM-on and REM-offcells. Recognition of these complexities forces us to revise the reciprocal-interaction model and to seek new methods to test its tenets.Cholinergic microinjection experiments indicate that some populations of REM-on cells can execute specific portions of the REM sleep syndrome or block the generation of REM sleep. This observation suggests that the order of activation within the anatomically distributed generator populations may be critical in determining behavioral outcome. Support for the cholinergic tenets of the reciprocal-interaction model has been reinforced by observations from sleep-disorders medicine.Specific predictions of the reciprocal-interaction model and suggestions for testing these predictions are enumerated for future experimental programs that aim to understand the cellular and molecular basis of the mammalian sleep cycle.

Evolving concepts of sleep cycle generation: From brain centers to neuronal populations

Increases in amino-cupric-silver staining of the supraoptic nucleus after sleep deprivation.

Comparison of the effects of two ‘sleep’ peptides, delta sleep-inducing peptide and arginine-vasotocin, on single neurons in the rat and rabbit brain stem

Arginine vasotocin (AVT), an alleged hormone of the mammalian pineal gland.

The role of nonapeptides in the modulation of sleep has been described by several studies; yet, little evidence is found on the effects on sleep of oxytocin (OT), a nonapetide involved in human social behaviour and in the regulation of the hypothalamo-pituitary-adrenal axis. The aim of the present study is to examine whether intranasal administration of OT has any effect on sleep architecture. Ten healthy male volunteers were included in a double-blind, cross-over study and were randomly administered nasal instillations of either placebo or OT. A one-month washout period was allowed between the administrations of each substance. Polysomnographic recordings were performed: before the beginning of drug administration, after seven days and after one month. We found that long-term administration of OT influences sleep architecture by reducing sleep latencies, increasing the sleep efficiency and increasing the percent of REM sleep episodes.

Intranasal administration of oxytocin alters sleep architecture

Arginine vasotocin (AVT) or placebo were subcutaneously administered to 4 men at 22.00 and 01.00 h, along four nights, and polygraphic recordings were performed between 22.00 and 02.00 h during sleep. AVT significantly increased only the amount of rapid eye movement (REM) sleep (p less than 0.05), but did not influence the latency of the first REM sleep period. This effect of AVT was not dose dependent in the range between 2 and 12 microgram AVT. AVT or placebo were also intravenously injected or perfused to 10 normal adult subjects, at different times of the day, under clinical control. Doses between 2 microgram perfused 4 h and 12 microgram perfused 30 min, did not produce clinical signs of sleep. It is suggested that AVT is not a blood factor for inducing of slow waves sleep (SWS) or REM sleep in humans.

Influence of arginine vasotocin administration on nocturnal sleep of human subjects.

Publisher Summary This chapter outlines the study of administration of arginine-vasotocin (AVT) to human subjects. As in mammals, synthetic arginine-vasotocin (AVT) produces marked effects on the secretion of the anterior pituitary and on sleep induction, especially when intraventricularly administered, but also intraperitoneally or intravenously, so that some authors consider AVT the most active substance in animal biology. In human subjects, in contrast to laboratory animals, synthetic AVT provided extremely small effects on the anterior pituitary as reflected by serum levels of adenohypophysial hormones and plasma level of 11-OHCS. In man, synthetic AVT prolongs the REM sleep periods and has no effects on the induction of sleep, contrary to the reported results on cats, in which AVT appears to be an extremely potent slow-wave sleep-inducing hormone, completely suppressing the REM. Another potential pineal hormone, the melatonin, also shows small and inconsistent endocrine effects when administered to human subjects and is likewise involved in sleep. These facts are probably explained by the different roles played by the pineal and during its phylogenetic evolution. The way of administration probably contributes to evidence these species differences.

Administration of arginine-vasotocin (AVT) to human subjects.

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Influence of arginine vasotocin administration on nocturnal sleep of human subjects.

Administration of arginine-vasotocin (AVT) to human subjects.