Multiple areas throughout the brain participate in the sleep–wake cycle. The waking state is maintained by a diffuse collection of neurons within the medulla, pons, midbrain, and diencephalons known as the reticular activating system. Electrical stimulation within the reticular activating system leads to a change in electroencephalogram pattern from the sleep state to that of the waking state—that is, cortical arousal. The sleep state does not result from the passive withdrawal of arousal but from two sleep centers that exist within the brain. One sleep center is responsible for producing slow-wave sleep, whereas the other produces rapid eye movement (REM) sleep.
The slow-wave sleep center is located within the medulla, in a midline area containing the raphe nuclei. Neurons within this nucleus use serotonin (5-hydroxytryptamine [5-HT]) as a neurotransmitter. Administration of 5-HT directly into the cerebral ventricles of expe-rimental animals induces a state of slow-wave sleep, whereas lesions in this region induce a permanent state of insomnia.
The REM sleep center is located in specific nuclei of the pontine reticular formation, including the locus ceruleus, which uses NE as a neurotransmitter. Lesions within this area eliminate the electrophysiological and behavioral signs of REM sleep. In adults, REM and non-REM sleep alternate through the night. In view of the important role of 5-HT and NE in sleep, it is understandable that drugs may affect the duration and/or content of sleep. Currently, very little is known regarding the neural control of nocturnal penile erec-tion. The current opinion is that reduced supraspinal inhibition of the spinal func-tion is partly involved in this process.