REM sleep

Measurement of movement of the eyeballs by means of electrodes placed adjacent to the eye sockets. The EOG parameter is important in defining REM sleep. Indeed, in animals sleep experiments where EOG data are not collected, the corresponding sleep state is most correctly termed paradoxical sleep. 

Figure 22.4 Idealised EEG-like patterns in sleep and waking. When we are awake and aroused the EEG is desynchronised (a). As we become drowsy and pass into sleep the EEG waves become more synchronised with 8-12 Hz alpha waves (b), sleep spindles then appear (c) before the EEG becomes even more synchronised with slow (about 1-2 Hz) high-voltage waves characteristic of deep slow-wave sleep (SWS). About every 90 min this pattern is disrupted and the EEG becomes more like that in arousal (d) except that the subject remains asleep. This phase of sleep is also characterised by rolling, rapid eye movements, the so-called REM sleep. SWS is consequently also known as non-REM sleep. These tracings have been drawn to show the main features of the different EEG phases of sleep and as such are much simpler than those that are actually recorded...

This sleep pattern, seen in adults, takes some time to develop and appears in infants only around 6 months to one year after birth. Instead, as new parents will testify, young babies have a sleep cycle that lasts only around 3-6 h. Further striking differences are that babies REM sleep accounts for as much as half the sleep cycle (compared with only a quarter in the adult) and is accompanied by increased motor activity with spasmodic movements of the limbs and facial muscles, rather than the muscle atonia seen in adults. In fact, the adult sleep cycle can take up to 20 years to stabilise and its pattern changes again in the elderly who show a reduction in the duration of SWS, an increase in the proportion of REM sleep, and increased daytime napping . 

The functions of these different phases of sleep are not at all clear but chronic sleep deprivation does eventually lead to death. It seems to be the slow-wave component of sleep (SWS) that is vital and it is thought to serve a restorative purpose. This would be consistent with its greater occurrence during the early stages of the sleep cycle when hormone secretion supports anabolic metabolism. If subjects are wakened every time they enter a period of REM sleep (evidenced by the EEG) there appears to be no overt harmful effect on their behaviour. In fact, REM sleep deprivation has even been used, with some claims of success, as a treatment for minor depression. However, there is an unproven belief that REM sleep is important for memory consolidation. 

Augment, or more probably, break up thalamic-cortico synchrony and its tendency to promote slow-wave EEG activity and non-REM sleep. Whether this results in full arousal, or merely a temporary disruption of sleep to give REM periods without full awaking, will depend on the balance of inputs and the overall state of cortical activity. 

In fact, there is a good deal of evidence to support this suggestion. First, more than half the neurons in the PPT fire rhythmically only when PGO waves are evident and their firing starts immediately before the PGO waves appear. Second, in cats, REM sleep is augmented by direct injection of either carbachol, or more selective muscarinic agonists, or the anticholinesterase, neostigmine, into the pontine reticular formation (one of the projection sites for PPT). Third, REM sleep is abolished by lesion of the PPT nucleus but, interestingly, not by lesion of the LDT. 

Overall, there are compelling reasons to believe that cholinergic pathways not only play a part in arousal but also contribute to the induction of the arousal-like features of REM sleep. 

Although histamine has mixed excitatory and inhibitory effects on central neurons, those antihistamines (Hi-receptor antagonists) that enter the brain produce sedation this indicates that the predominant overall effect of histamine is excitatory. The preferred explanation for this rests on evidence that histaminergic neurons in the posterior hypothalamus are active in waking and silent in deep SWS and REM sleep. 

A link between 5-HT release and increased waking is supported by evidence from in vivo microdialysis of cats and rats. This has confirmed that the extracellular concentration of 5-HT in all brain regions studied to date is lower during both SWS and REM sleep than in the awake state (see Portas, Bjorvatn and Ursin 2000). Interestingly, if behaviour is maintained at a constant level, the activity of 5-HT neurons does not show circadian variation although 5-HT turnover in the brain areas to which they project... 

Administration of 5-HTib receptor agonists increases waking time and reduces REM sleep. This is consistent with recent evidence gathered from 5-HTiB-receptor knockout mice which exhibit more REM sleep and less SWS than the wild-type. Moreover, 5-HTib agonists reduce, while antagonists increase, REM sleep in the wild-type mouse, but neither type of compound has any effect in the knock-outs (Boutrel et al. 1999). Unfortunately, it is not known whether these actions are mediated by presynaptic, postsynaptic or heteroceptors and therefore whether 5-HT activity is increased or decreased. It is also not helped by the limited selectivity of test agents. 

Figure 22.9 Summary of the influence of varying factors on sleep and waking. The EEG is shown diagramatically in the typical arousal (awake) state and in both non-REM (slow wave) and REM sleep. Appropriate activity levels, high or low, are shown for the different factors such as light input, melatonin secretion or ACh, NA, and 5-HT function in the different phases...

---