Rapid eye movement sleep
|Title||Rapid eye movement sleep|
|Publication Type||Book Chapter|
|Year of Publication||2017|
|Book Title||Principles and Practice of Sleep Medicine|
Rapid eye movement (REM) sleep was first identified by its most obvious feature: rapid eye movements occurring during sleep. In most adult mammals the electroencephalogram (EEG) of the neocortex is low in voltage during REM sleep. The hippocampus exhibits regular high-voltage theta waves throughout REM sleep. The key brain structure for generating REM sleep is the brainstem, particularly the pons and adjacent portions of the caudal midbrain. The isolated brainstem can generate REM sleep, including rapid eye movements, spike potentials linked to eye movements called pontogeniculo- occipital (PGO) waves, muscle tone suppression (atonia), and autonomic variability. The structures rostral to the caudal midbrain– pontine brainstem cannot generate the forebrain aspects of REM sleep, such as PGO waves or rapid eye movements. The brainstem and the hypothalamus contain cells that are maximally active in REM sleep, called “REM-on cells,” and cells that are minimally active in REM sleep, called “REM-off cells.” Subgroups of REM-on cells each use a specific transmitter— gamma-aminobutyric acid (GABA), acetylcholine, glutamate, or glycine. Subgroups of REM-off cells use the transmitters norepinephrine, epinephrine, serotonin, histamine, and GABA. Destruction of large regions within the midbrain and pons can prevent the occurrence of REM sleep. More limited damage to portions of the brainstem can cause abnormalities in certain aspects of REM sleep. Of particular interest are manipulations that affect the regulation of muscle tone within REM sleep. Early animal work found that lesions of several regions in the pons and medulla can cause REM sleep to occur without the normal loss of muscle tone. In REM sleep without atonia, animals exhibit locomotor activity, appear to attack imaginary objects, and execute other motor programs during a state that otherwise resembles REM sleep. Subsequent work found a similar syndrome in humans that has been termed the REM sleep behavior disorder. Stimulation of portions of the REM sleep–controlling area of the pons can produce a loss of muscle tone in antigravity and respiratory musculature during waking, without eliciting all aspects of REM sleep. Narcolepsy is characterized by abnormalities in the regulation of REM sleep. Most cases of human narcolepsy are caused by a loss of hypocretin (orexin) neurons. Hypocretin neurons, which are located in the hypothalamus, contribute to the regulation of the activity of norepinephrine, serotonin, histamine, acetylcholine, glutamate, and GABA cell groups. Hypocretin neurons have potent effects on alertness and motor control and normally are activated in relation to particular, generally positive, emotions in humans as well as in animals.