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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.
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.
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.
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