Physiology of rem sleep

During REM sleep GABAergic inhibition comes from a various source, REM- on cells, possibly located in the periaqueductal gray matter. These shut down the serotonergic and noradrenergic (wake-on/REM-off) neurons but not the orexin cells. Now, pontine cholinergic wake-on or REM-on cells is activated through the combination of continued excitation through orexinergic cells plus disinhibition from the aminergic neurons. In significant:

- High levels of actions in these cholinergic neurons will causes depolarization of the thalamic relay neurons that go into tonic firing mode.

- The continual action of the orexin neurons keeps the basal forebrain cholinergic cells responsive.Both effects conspire to desynchronize the EEG.

The pontine cholinergic neurons also organize—via relays through pontine and medullary reticular nuclei—two major features of REM sleep. The first is the powerful suppression of sensory input and motor output. Presynaptic GABAergic inhibition on afferent terminals reduces sensory input. Glycinergic postsynaptic inhibition of motor neurons is the route by which muscle atonia (loss of muscle tone) is brought about. Thus, during REM sleep the brain is uncoupled from the external world; it is “off-line.” Lesions of the pons which prevent the muscle atonia produce animals which express stereotyped behaviors in the duration of REM sleep. This suggests that during normal REM sleep motor patterns are generated but not executed; we cannot act out our dreams.

A second major feature of REM sleep are periodic pontine geniculate-occipital (PGO) spikes in the EEG. These originate from cholinergic cells in the pons. They drive reticular and vestibular neurons to excite oculomotor neurons by causing the rapid eye movements and other cells to produce the phasic alterations in blood flow, heart rate, respiration and muscle twitches seen in REM sleep. The PGO-on cells also initiate the spread of activity to the lateral geniculate nucleus and visual cortex recorded as PGO spikes. During wakefulness PGO-on cells are commonly inhibited through serotonergic cells although, PGO spikes can be produced in awake subjects through sudden stimuli so they may underlie startle responses.

It is not  known what  causes the brain to switch from  NREM to REM sleep  and  back  various times during the  night and  there are various candidates for the  GABAergic neurons which trigger  REM sleep. Although, it is thought which orexigenic neurons stabilize the waking or REM state once the brain has made the transition. This idea is supported through the discovery of deficits in orexin neurotransmission in humans and animals with narcolepsy. In this situation patients experience frequent and undesired flips into REM sleep during the day.