Rapid eye movement sleep for sleep monitoring

Rapid eye movement sleep for sleep monitoring

REM sleep (REM)

The EEG amplitude is reduced similarly to the awakening, the new cortex exhibits a low voltage, and the hippocampus exhibits a regular high voltage θ wave;

Slow muscle tone;

Genital erection, expansion changes;

The body temperature regulation disappears and the body temperature fluctuates with the ambient temperature;

The lateral geniculate PGO wave maps to the thalamic nucleus and the neocortex (ponto – geniculo - occipital PGO);

Irregular heart rate (irregular activity is not controlled by a single pacemaker);

Produce peripheral or middle ear muscle twitching signals that may precede or be secondary to PGO and rapid eye movement;

Clear and vivid "dreams."

REM generation mechanism

★ disconnect research

The pons is a key part of REM sleep and is the result of dynamic interaction between the forebrain and brainstem mechanisms. Deletion of muscle tone requires activation of the motor inhibition system in the spinal cord;

★ Damage research

Deletion of the under-blue nucleus

★Stimulation research

Cholinergic agonists stimulate the strongest form of REM sleep (injected into specific parts of the ventral blue plaque of the pons

★ neuron activity

REM-distribution cells (REM-priming): the neurotransmitters that release the cell population are gamma-aminobutyric acid, acetylcholine, glutamic acid or glycine;

REM-quiet cells (REM-off): the neurotransmitters that release the cell population are norepinephrine, adrenaline, serotonin and histamine;

Muscle tension control

During REM sleep, inhibition of motor output is accompanied by inhibition of sensory transmission, and both have similar neurological mechanisms.

REM sleep function

Evolutionary perspective:

Arousal from REM sleep is more alert than NREM, and the inactivation state of NREM leads to slower metabolic processes and lower response.

REM rebound phenomenon:

During REM sleep, histamine, norepinephrine, and serotonin neurons are terminated, and this termination does not occur in the awake state, so waking is not a substitute for REM sleep function.

Rebound may be the accumulation of demand for monoaminergic cell population passivation. When the release is reduced, the synthesis of monoamines and receptors is accelerated, and agonists are not required, and the receptors of these substances can be desensitized. But this hypothesis is not fully supported.

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