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The discovery of rapid eye movement (REM) sleep revolutionized the field of sleep research. REM sleep is that state in which most of our dreams occur. During REM sleep, the brain is active, while the body is asleep. These characteristics make REM sleep a unique and a paradoxical state. While we are struggling to understand the function of REM sleep, major advances have been made in understanding the cellular mechanisms responsible for REM-sleep control. In this chapter, we have described two neurochemical substrates involved in REM-sleep regulation. One of them is adenosine and the other is glycine.
Adenosine is implicated to be the homeostatic regulator of sleep. It has been suggested that adenosine acts via A1 receptors to inhibit wake-promoting neurons and promote the transition from wakefulness to sleep. Adenosine acts on multiple wake-promoting systems including the basal forebrain cholinergic and the non-cholinergic systems, namely the orexinergic, and the histaminergic systems. There are reports suggesting that adenosine may act via A2A receptors and activate sleep-promoting neurons of the preoptic region. In addition, studies suggest a direct role of adenosine in the modulation of REM sleep.
During REM sleep, there is a tonic muscle atonia coupled with phasic muscle twitches. This phenomenon is regulated by the dorsolateral pons and ventromedial medulla along with local neurons within the spinal cord. Glycinergic mechanisms are responsible for the control of muscle tone during REM sleep. However, the exact role is under debate.
Since the dawn of civilization, sleep has fascinated humankind. Myriad treatises and reviews, scientific and nonscientific, have been written in an attempt to explain the phenomenon of sleep, yet none has been comprehensive enough to gain general acceptance. It is now well established that sleep is neither a unitary nor a passive process. Intricate neuronal systems via complex mechanisms are responsible for controlling sleep. This chapter focuses on the evolution of rapid-eye-movement (REM) sleep; for detailed information about other behavioral states, the reader is referred to several comprehensive reviews (Datta & Maclean, 2007; Jones, 2003; Mignot, 2004; Siegel, 2004; Steriade & McCarley, 2005). We begin with a brief description of the discovery of REM sleep and then describe the phylogeny and evolution of REM.
Discovery of REM sleep
The discovery of REM sleep, a major breakthrough, revolutionized the field of sleep research. The process that led to this discovery began in Kleitman's laboratory at the University of Chicago Medical School in 1953. Kleitman and his graduate student Eugene Aserinsky noticed rhythms in eye movements during sleep in humans and linked this to dreaming (Aserinsky & Kleitman, 1953, 1955). Subsequently, Dement and Kleitman (1957) characterized the electroencephalographic (EEG) activity during dreaming in humans, and later Dement (1958) recorded rapid eye movements during sleep in animals. These discoveries established the presence of the non-REM–REM sleep cycle.
Wakefulness is a prerequisite for survival and is accompanied by an ensemble of other behaviors. Thus, the brain contains multiple and grossly redundant systems controlling wakefulness: the histaminergic system is one of them. The histaminergic system in the central nervous system (CNS) is exclusively localized within the tuberomammillary nucleus (TMN). It consists of histamine-containing neurons that innervate almost all the major regions of the CNS, including the spinal cord. Within the CNS, histamine mediates its effects via three G-protein coupled metabotropic receptors: the H1, H2, and H3 receptors. Of these three receptors, the H3 receptor functions as an autoreceptor and regulates the synthesis and release of histamine. The histaminergic system, like other monoaminergic systems, is implicated in the regulation of sleep–wakefulness. It has been suggested that TMN neurons are under inhibitory control of the sleep-inducing ventrolateral preoptic GABAergic neurons and induce wakefulness by activating the wakefulness-promoting cholinergic neurons of the basal forebrain via the H1 receptor. Although the bulk of evidence is derived from pharmacological studies, numerous electrophysiological and biochemical studies also support the role of histamine in wakefulness.
Electrophysiological evidence suggests that the histaminergic neurons, like other monoaminergic neurons, have their highest discharge during wakefulness. Biochemical evidence also suggests that histamine release in the TMN and other target regions is highest during wakefulness.
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