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Chapter: Medical Physiology: States of Brain Activity-Sleep, Brain Waves, Epilepsy, Psychoses

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Basic Theories of Sleep

Sleep Is Believed to Be Caused by an Active Inhibitory Process.

Basic Theories of Sleep

Sleep Is Believed to Be Caused by an Active Inhibitory Process.

An earlier theory of sleep was that the excitatory areas of the upper brain stem, the reticular activating system, simply fatigued during the waking day and became inactive as a result. This was called the passive theoryof sleep. An important experiment changed this viewto the current belief that sleep is caused by an activeinhibitory process: it was discovered that transectingthe brain stem at the level of the midpons creates a brain whose cortex never goes to sleep. In other words, there seems to be some center located below the mid-pontile level of the brain stem that is required to cause sleep by inhibiting other parts of the brain.

Neuronal Centers, Neurohumoral Substances, and Mechanisms That Can Cause Sleep— A Possible Specific Role for Serotonin

Stimulation of several specific areas of the brain can produce sleep with characteristics near those of natural sleep. Some of these areas are the following:

1.The most conspicuous stimulation area for causing almost natural sleep is the raphe nuclei in thelower half of the pons and in the medulla. Thesenuclei are a thin sheet of special neurons located in the midline. Nerve fibers from these nuclei spread locally in the brain stem reticular formation and also upward into the thalamus, hypothalamus, most areas of the limbic system, and even the neocortex of the cerebrum. In addition, fibers extend downward into the spinal cord, terminating in the posterior horns where they can inhibit incoming sensory signals, including pain. It is also known that many nerve endings of fibers from these raphe neurons secrete serotonin. When a drug that blocks the formation of serotonin is administered to an animal, the animal often cannot sleep for the next several days. Therefore, it has been assumed that serotonin is a transmitter substance associated with production of sleep.

 

2.Stimulation of some areas in the nucleus of thetractus solitarius can also cause sleep. This nucleusis the termination in the medulla and pons for visceral sensory signals entering by way of the vagus and glossopharyngeal nerves.

 

3.Stimulation of several regions in the diencephalon can also promote sleep, including (1) the rostral part of the hypothalamus, mainly in the suprachiasmal area, and (2) an occasional area in the diffuse nuclei of the thalamus.

 

Lesions in Sleep-Promoting Centers Can Cause Intense Wake-fulness. Discrete lesions in theraphe nucleilead to ahigh state of wakefulness. This is also true of bilateral lesions in the medial rostral suprachiasmal area in theanterior hypothalamus. In both instances, the excita-tory reticular nuclei of the mesencephalon and upper pons seem to become released from inhibition, thus causing the intense wakefulness. Indeed, sometimes lesions of the anterior hypothalamus can cause such intense wakefulness that the animal actually dies of exhaustion.

Other Possible TransmitterSubstances Related to Sleep.

Experiments have shown that the cerebrospinal fluid as well as the blood or urine of animals that have been kept awake for several days contains a substance or substances that will cause sleep when injected into the brain ventricular system of another animal. One likely substance has been identified as muramyl peptide, a low-molecular-weight substance that accumulates in the cerebrospinal fluid and urine in animals kept awake for several days. When only micrograms of this sleep-producing substance are injected into the third ventricle, almost natural sleep occurs within a few minutes, and the animal may stay asleep for several hours. Another substance that has similar effects in causing sleep is a nonapeptide isolated from the blood of sleeping animals. And still a third sleep factor, not yet identified molecularly, has been isolated from the neuronal tissues of the brain stem of animals kept awake for days. It is possible that prolonged wakeful-ness causes progressive accumulation of a sleep factor or factors in the brain stem or in the cerebrospinal fluid that lead to sleep.

Possible Cause of REM Sleep. Why slow-wave sleep isbroken periodically by REM sleep is not understood. However, drugs that mimic the action of acetylcholine increase the occurrence of REM sleep. Therefore, it has been postulated that the large acetylcholine-secreting neurons in the upper brain stem reticular for-mation might, through their extensive efferent fibers, activate many portions of the brain. This theoretically could cause the excess activity that occurs in certain brain regions in REM sleep, even though the signals are not channeled appropriately in the brain to cause normal conscious awareness that is characteristic of wakefulness.

Cycle Between Sleep and Wakefulness

The preceding discussions have merely identified neuronal areas, transmitters, and mechanisms that are related to sleep. They have not explained the cyclical, reciprocal operation of the sleep-wakefulness cycle. There is as yet no explanation. Therefore, we can let our imaginations run wild and suggest the following possible mechanism for causing the sleep-wakefulness cycle.

When the sleep centers are not activated, the mes-encephalic and upper pontile reticular activating nuclei are released from inhibition, which allows the reticular activating nuclei to become spontaneously active. This in turn excites both the cerebral cortex and the peripheral nervous system, both of which send numerous positive feedback signals back to the same reticular activating nuclei to activate them still further. Therefore, once wakefulness begins, it has a natural tendency to sustain itself because of all this positive feedback activity.

Then, after the brain remains activated for many hours, even the neurons themselves in the activating system presumably become fatigued. Consequently, the positive feedback cycle between the mesen-cephalic reticular nuclei and the cerebral cortex fades, and the sleep-promoting effects of the sleep centers take over, leading to rapid transition from wakefulness back to sleep.

This overall theory could explain the rapid transi-tions from sleep to wakefulness and from wakefulness to sleep. It could also explain arousal, the insomnia that occurs when a person’s mind becomes preoccu-pied with a thought, and the wakefulness that is pro-duced by bodily physical activity.


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