Rapid eye movement sleep

Rapid eye movement sleep (REM sleep, REMS) is a unique phase of sleep characterized by rapid movement of the eyes, low muscle tone throughout the body, and the propensity of the sleeper to dream vividly. This phase is also known as paradoxical sleep (PS) and sometimes desynchronized sleep because of physiological similarities to waking states, including rapid, low-voltage desynchronized brain waves. Electrical and chemical activity regulating this phase seems to originate in the brain stem and is characterized most notably by an abundance of the neurotransmitter acetylcholine, combined with a nearly complete absence of monoamine neurotransmitters histamine, serotonin, and norepinephrine. The cortical and thalamic neurons of the waking or paradoxically sleeping brain are more depolarized—i.e., can "fire" more readily—than in the deeply sleeping brain. The right and left hemispheres of the brain are more coherent in REM sleep, especially during lucid dreams.

REM sleep is punctuated and immediately preceded by PGO (ponto-geniculo-occipital) waves, bursts of electrical activity originating in the brain stem. These waves occur in clusters about every 6 seconds for 1–2 minutes during the transition from deep to paradoxical sleep. They exhibit their highest amplitude upon moving into the visual cortex and are a cause of the "rapid eye movements" in paradoxical sleep.

Brain energy use in REM sleep, as measured by oxygen and glucose metabolism, equals or exceeds energy use in waking. The rate in non-REM sleep is 11–40% lower.

Compared to slow-wave sleep, both waking and paradoxical sleep involve higher use of the neurotransmitter acetylcholine, which may cause the faster brainwaves. The monoamine neurotransmitters norepinephrine, serotonin and histamine are completely unavailable. Injections of acetylcholinesterase inhibitor, which effectively increases available acetylcholine, have been found to induce paradoxical sleep in humans and other animals already in slow-wave sleep. Carbachol, which mimics the effect of acetylcholine on neurons, has a similar influence. In waking humans, the same injections produce paradoxical sleep only if the monoamine neurotransmitters have already been depleted.

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