Summary

Research into the influence of monoamines on REM sleep-generating processes began as early as 1964, 11 years after the discovery of REM sleep. Various studies have now established that noradrenergic neurons of the locus coeruleus must be silent for REM sleep to occur. However, the maintenance of a low level of noradrenaline is still necessary. This phenomenon is linked to the persistence of noradrenaline in the brain resulting from its diffuse release at the varicosity level and the absence of rapid noradrenaline elimination by reuptake and enzymatic destruction. The role of dopamine in the regulation of REM sleep was discovered more recently. The infusion of dopamine agonists into the REM sleep-inducing structure called the peri-locus coeruleus-α inhibits REM sleep. However, this effect can be blocked by the concurrent administration of dopamine antagonists, indicating a basic noradrenergic function. In the same way, lesions of the dopaminergic ventral periaqueductal gray matter increase REM sleep. Serotonergic neurons become silent during REM sleep, and serotonin, which is involved in processes that support waking, also has REM sleep-off influences. Finally, histamine appears to have indirect influences on REM sleep, as histaminergic neurons become silent as soon as sleep onset occurs. This monoamine acts in connection with orexin, a deficit of which favors REM sleep and narcolepsy. The narcoleptic attacks seen in knock-out mice lacking orexin can be prevented by antagonists of the H3 histamine autoreceptor.