Preface

Since the publication of the first edition of Rapid Eye Movement Sleep (Mallick and Inoue, 1999), the advances in the field of sleep research have been phenomenal; in particular, those concerning rapid eye movement (REM) sleep. The emphasis on REM sleep may be gauged by the fact that recently a conference exclusively devoted to this subject was organized in France to celebrate 50 years since the discovery of REM sleep as well as to honor Professor Michel Jouvet, a pioneer and one of the doyens in this field.

Summary

Sleep has been generally divided into rapid eye movement (REM) sleep and non-REM (NREM) sleep in higher order mammals, including humans. Several theories have proposed various functions of different stages of sleep. We hypothesized that REM sleep maintains brain excitability. In this chapter, we discuss the significance of REM sleep in the maintenance of neuronal electrochemical homeostasis, which governs brain excitability. Selective REM-sleep loss increases the activity of Na-K ATPase, a membrane-bound enzyme that maintains neuronal Na+ and K+ homeostasis and, thus, the neuronal resting membrane potential. Further, the REM sleep deprivation-induced increase in Na-K ATPase activity has been attributed to an increased level of norepinephrine in the brain.

Summary

Dreams have been known to mankind from time immemorial, while rapid eye movement sleep (REMS) has been objectively defined by characteristic electrophysiological signals since the mid twentieth century only. In the absence of better objective criteria, modern experimental sleep neurobiologists have objectively identified the dream state of a subject with REMS; thus, the dream state and REMS have often been used synonymously. There are reasons to believe that those states are not exclusively correlated to each other, rather they are independent phenomena that are often expressed simultaneously; however, neurobiological explanations are still lacking. In an attempt to better understand the relationship between them, we combined findings from objective science such as non-locality in physics with that of subjective science such as the phenomenon of consciousness. We explored the wisdom in the Upanishads, especially those instances where these ancient writings refer to sleep, dream, and states of consciousness, and attempted to offer an explanation based on modern experimental science. Our search led us towards a conceptual novelty in proposing the existence of an all-inclusive basal ground state (T or Turiya), which possibly equates to very slow waves in the electroencephalogram (EEG), during which waking, dream, non-REMS (NREMS), and REMS express apparently as independent phenomena, though overlapping to various degrees on many occasions. The proposed hypothesis and model, unlike several other earlier ones, is based on known and rational physiological principles, and hence is amenable to experimental verification.

Summary

The brain-stem cholinergic neurons, having higher activity during rapid eye movement (REM) sleep, located in several isolated nuclei are known as REM-on neurons. In contrast, the monoaminergic neurons in the brain stem and in the forebrain areas exhibit higher activity during wakefulness, almost completely cease their firing during REM sleep and have been termed as REM-off neurons. The norepinephrin (NE)-ergic neurons located in the locus coeruleus (LC) could be the negative REM sleep-executive neurons and their cessation during REM sleep seems to be obligatory for its occurrence. Our findings that the wakefulness-promoting neurons are inhibitory to REM-on neurons and excitatory to the REM-off neurons led us to suggest that the wakefulness-related neurons do not allow REM sleep to occur and cessation of REM-off neurons is a necessity for the generation of REM sleep. The caudal brain-stem reticular formation (CRF), which induces cortical synchronization, facilitates the activity of REM-on neurons. However, the hypothalamic non-REM sleep-related neurons do not seem to have significant effect on the spontaneous activity of the REM-on neurons, although they may be indirectly modulating REM sleep. Taken together these findings suggest that normally waking neurons do not allow REM sleep to appear; at a certain depth of non-REM sleep the CRF facilitates the onset of REM sleep and re-activation of the wake-active neurons in the brain stem is requisite for its termination.

Abstract

Aserinsky & Kleitman (1953) identified within sleep a physiological state that expresses several signs apparently similar to those that occur during wakefulness. This state was termed rapid eye movement (REM) sleep. REM sleep may play a significant role in maintaining normal physiological functions, as its loss has serious detrimental psychopathological effects. The mechanism of REM sleep regulation is still unknown. The pontine cholinergic and noradrenergic transmissions in the brain undergo reciprocal variations in activity associated with the transformation from non-REM sleep to a REM sleep state and vice versa. The cessation of noradrenergic neuronal firing in the locus coeruleus (LC) plays a crucial role in the regulation of REM sleep. Disinhibition of the LC neurons may result in increased levels of noradrenaline (NA) in the brain, and this increased brain NA is likely to be responsible for the pathophysiological effects associated with REM sleep deprivation. Based on recent findings, we discuss the modulation as well as the role of LC neurons and NA in the modulation of REM sleep and the pathophysiological conditions associated with its deprivation. We propose that LC NA neurons are negative executive neurons for the regulation of REM sleep.

Introduction

One of the important characteristics of living beings is to alternate between active and rest phases, but the underlying mechanism/s and functions are not yet known.