ABSTRACT
For years, sleep was explained as a passive phenomenon: the gradual running down of the wakefulness-maintaining system until it reached a state of inactivity, i.e., sleep. Much controversy has developed over the possibility of the existence of sleep factors or substances which will produce sleep when injected into an animal and will cause a maintenance of wakefulness when deprived or blocked at certain active brain sites. The inhibitory brain chemical involved appears to be the neurotransmitter gamma-aminobutyric acid (GABA). In Hartmann's theory, rapid eye movement (REM) sleep functions to maintain the brain catecholamine system at a certain homeostatic, optimum level of performance. The cells of the medial pontine reticular formation experience a gradual depolarization in membrane potential just prior to REM sleep. More recent and detailed studies suggest that the Electroencephalograph (EEG) de-synchronization of REM sleep is mediated by cholinoceptive cells in the midbrain reticular formation.
