The Neurophysiology and Neurochemistry of Sleep


By Sergey Skudaev

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It is known that sleep is very important for health and essential for surviving. Sleep deprivation leads to death within three weeks. However the purpose of sleep is still not clearly understood. Two fundamental processes carry out regulation of sleep: circadian rhythm and homeostasis.

Circadian rhythm determines the temporal organization of the daily activity of the hormonal and nervous system. For example, rats are awake at night and sleep during the day.

Homeostatic mechanisms restore deviations in body conditions caused by environmental stimuli or endogenous processes. For example, prolonged wakefulness increases the length of sleep. Krueger J.M et al 1998

At the beginning of 20th century, scientists believed that sleep is a rest state of our brain and body. In 1950s it was discovered that brain activity, brain blood flow; blood pressure and heart rate in some sleep stages might be the same as when awake.

No longer is sleep considered as a passive condition or as an absent of wakefulness. Brain cell activity is not inhibited, but reorganized in sleep. Cells of the cerebral cortex in sleep are united in synchronized activity (chorus), while in wake state some cells are inhibited, and some are active.

It has been shown that sleep is essential for adaptation to stress and to learning. Consolidation of short-term memory in long term takes place in sleep. While asleep, our brain is planning our future actions and is testing their outcomes.

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Sleep states and stages

Sleep consists of two different states: Non-REM sleep and REM sleep. REM stands for Rapid Eye Movement. EEG is a recording of electrical brain activity. To register EEG, electrical wires with silver contacts are applied to the patient´s scalp or brain surface and connected to an amplifier and a recording device. The procedure of recording EEG is similar to that of EKG.

The first human EEG was recorded by Hans Berger in 1924. He proved that EEG waves are generated by the brain. His work was published in 1929[1]. The EEG waves are formed as a result of summation of individual neuron activity. The more synchronized neuronal activity, the higher voltage waves are registered in EEG. The less synchronized neuronal activity, the lower the EEG waves are.

A normal EEG of a relaxed person who closed his/her eyes usually displays well-synchronized waves with frequency around 10 per second and an amplitude about of approximately 50 micro volts. These waves are called alpha waves or alpha rhythms. A light or sound stimuli cause desynchronization of the EEG; alpha waves are replaced with low voltage and high frequency beta waves. Beta waves may appear without external stimuli, when a person performs a calculation or is involved in some other activity. Grey Walter [] 1952.

During sleep, EEG waves are changing from high frequency and low voltage to low frequency and high voltage (synchronization of neuronal activity). After approximately 70-80 minutes of sleep, the EEG becomes similar to that in wake state; blood flow through the brain increases, tonus of skeletal muscles dramatically drops, and rapid eye movement (REM) is observed. This state of sleep is called REM sleep. Persons who wake up in REM sleep describe vivid colorful visual dreams. REM sleep is also called Fast-Waves Sleep, while Non-REM sleep is called Slow Waves Sleep.

Two graduate students, Eugene Aserinsky and Nathaniel Kleitman, from the laboratory of William C. Dement [] at the University of Chicago discovered and described REM sleep in the early 50s. At birth, REM sleep composes 90% of the total amount of sleep.

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Sleep in adult human comprises of 90 minutes cycles of Non-REM and REM sleep. REM sleep constitutes about 20% of total sleep time. The first REM sleep episode lasts about 5-10 minutes. The length of the REM sleep phase increases toward the morning.

Deprivation of REM sleep during one night leads to increasing the total REM sleep the next night. Long deprivation of REM sleep may cause hallucination and psychotic disorders.

The muscle atonia in REM sleep increases resistance of the upper airway and as a result obstructive sleep apnea (OSA) may occur in some individuals. OSA is characterized by the frequent temporary interruption of breathing during sleep. Inhibition of hypoglossal motoneurons, which control tongue movement, may contribute to OSA during REM sleep. Bellingham M. C, Funk G.D [] (2000). It is believed that Sudden Infant Death Syndrome (SIDS) also occurs in REM sleep.

Deprivation of REM sleeps in rats for as long as 20 days causes loss of weight in spite of increased food consumption. M. Koban and K. L. Swinson [] 2005. REM sleep deprivation in rats usually is achieved with a very simple method. A flowerpot is placed upside down in bath with water. A rat is sat on the top of the flowerpot. In the REM sleep stage rat muscles are losing tonus and as a result, the rat falls in the water and wakes up. Then it climbs back on the top of the flowerpot and may sleep in Non-REM stage until it falls in the water in the next REM stage. REM sleep deprived rat metabolism rose to 166% of baseline.

Non-REM sleep consists of four stages. A. Rechtschaffen, J. Siegel [] 2000. The first stage of sleep is characterized by transition from wakefulness to sleep. It lasts few minutes. EEG of the first stage shows low-amplitude mix frequency waves.

EEG in the second stage shows periods of well-synchronized sinusoidal waves at 12-14 per second. Due to their shape they are called sleep spindles.

In the third sleep stage slow, high-amplitude waves appear in the EEG every 0.5-2 seconds.

The fourth stage is characterized by dominating slow high-amplitude waves. In 3 and 4 stages of sleep neuronal activity, blood pressure and heart rate is low.

Global decrease of cerebral blood flow (CBF), oxygen and glucose metabolism are observed in slow wave sleep (SWS). No difference in CBF, oxygen and glucose metabolism were observed between REM sleep and wakefulness. Regional cerebral blood flow (rCBF ) was significantly decreased in the pons, midbrain, thalamus and basal forebrain during SWS. There was no significant decrease of CBF in primary or secondary sensory cortex, which implies that sensory systems remain functional during the sleep. Kajimura N. et al. 1999. Hofle N et al. 1997.

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