REM sleep activity

When we speak of REM sleep activation of the limbic, paralimbic, and subthalamic brain—and ascribe such dream emotions as elation, anxiety, and anger to it—we may sound a bit Ercudian. When all is said and done, isn t this Ereud s id, getting stirred up in sleep and raising havoc with... 

That adverse consequences would arise—were it not for the active inhibition of movement—is made dramatically clear by patients who lose their innate ability to block other motor outputs and hence enact their sometimes self-injurious dream scenarios. We will come back to this story when we discuss the tendency of some legally prescribed, consciousness altering drugs to mimic those CNS degenerative diseases that cause this so-called REM sleep behavior disorder. The one motor system whose REM sleep activation results in real, not fictive movement is, of course, the one that moves the eyes rapidly, giving REM its name. There is no need to inhibit this system, because its motor output creates no behavioral disruption of sleep or other adverse consequences for the dreamer. 

When we take PGO waves to be evidence of cholinergically mediated phasic activation, we can suggest that the frontal cortex is the one area of the cat brain that is selectively deprived of this distinctive REM sleep activation process. Here again, a comparative study, using fMRI imaging, might yield surprisingly consonant results. 

Now we must recall that regional brain analysis of diminished psychological function in dreaming shows an association with the lack of noradrenaline and serotonin in the REM sleep-activated brain - these two chemicals are known to be necessary for attention, learning, and memory (and by implication for orientation and... 

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 . 

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. 

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...

Non-REM sleep A state of usually dreamless sleep that occurs regularly during a normal period of sleep with intervening periods of rapid eye movement (REM) sleep and that consists of four distinct substages and low levels of autonomic physiologic activity. 

Rapid eye movement (REM) sleep A state of sleep that recurs cyclically several times during a normal period of sleep and is characterized by increased neuronal activity of the forebrain and midbrain, by depressed muscle tone, and especially in humans by dreaming, rapid eye movements, and vascular congestion of the sex organs. 

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