Music : Rapid Eye Movement Sleep

                               Rapid Eye Movement Sleep

Rapid eye movement sleep (REM sleep) is a normal stage of sleep characterized by the rapid and random movement of the eyes. REM sleep is classified into two categories: tonic and phasic. It was identified and defined by Nathaniel Kleitman, Eugene Aserinsky, and Jon Birtwell in the early 1950s. Criteria for REM sleep includes rapid eye movement, but also low muscle tone and a rapid, low-voltage EEG; these features are easily discernible in a polysomnogram, the sleep study typically done for patients with suspected sleep disorders.

Physiologically, certain neurons in the brain stem, known as REM sleep-on cells, (located in the pontine tegmentum), are particularly active during REM sleep, and are probably responsible for its occurrence. The release of certain neurotransmitters, the monoamines (norepinephrine, serotonin and histamine), is completely shut down during REM.This causesREM atonia, a state in which the motor neurons are not stimulated and thus the body’s muscles do not move. Lack of such REM atonia causes REM behavior disorder; sufferers act out the movements occurring in their dreams. Heart rate and breathing rate are irregular during REM sleep, again similar to the waking hours.

According to “scanning hypothesis” the directional properties of REM sleep eye movements are related to shifts of gaze in dream imagery. Against this hypothesis is that such eye movements occur in those born blind and in fetuses in spite of lack of vision. Also, binocular REMs are non-conjugated and so lack a fixation point. In support, research finds that in goal-oriented dreams, eye gaze is directed towards the action described by the dreamer.

Sleep aids the process by which creativity forms associative elements into new combinations that are useful or meet some requirement.This occurs in REM sleep rather than in NREM sleep.Rather than being due to memory processes, this has been attributed to changes during REM sleep in cholinergic and noradrenergic neuromodulation. During REM sleep, high levels of acetylcholine in the hippocampus suppress feedback from hippocampus to the neocortex, and lower levels of acetylcholine and norepinephrine in the neocortex encourage the spread of associational activity within neocortical areas without control from the hippocampus.This is in contrast to waking consciousness, where higher levels of norepinephrine and acetylcholine inhibit recurrent connections in the neocortex. REM sleep through this process adds creativity by allowing “neocortical structures to reorganise associative hierarchies, in which information from the hippocampus would be reinterpreted in relation to previous semantic representations or nodes.”

It has been suggested that acute REM sleep deprivation can improve certain types of depression when depression appears to be related to an imbalance of certain neurotransmitters. Although sleep deprivation in general annoys most of the population, it has repeatedly been shown to alleviate depression, albeit temporarily.More than half the individuals who experience this relief report it to be rendered ineffective after sleeping the following night. Thus, researchers have devised methods such as altering the sleep schedule for a span of days following a REM deprivation periodand combining sleep-schedule alterations with pharmacotherapyto prolong this effect. Though most antidepressants selectively inhibit REM sleep due to their action on monoamines, this effect decreases after long-term use. It is interesting to note that REM sleep deprivation stimulates hippocampal neurogenesis much the same as antidepressants.

R.E.M.