Abstract
In humans, slow-wave sleep (SWS) consists of stages 3 and 4 of non rapid eye movement (nonREM) sleep. The low-frequency, high-amplitude slow waves that dominate the electroencephalogram (EEG) during SWS can be quantified as slow-wave activity (SWA). SWS and SWA are regulated very accurately in response to variations in the duration and intensity of wakefulness and sleep. SWA declines more or less independently of circadian phase during the course of a sleep episode, indicating that it is primarily under homeostatic rather than circadian control. An age-related decline in SWS and SWA is well established. In some studies, apprehension, depression and insomnia have been associated with reductions in SWS and SWA. Experimental reductions of SWS through SWS deprivation (without altering total sleep time or REM duration) have been reported to lead to an increase in daytime sleep propensity and reductions in performance. SWS and SWA are therefore thought to contribute to the recovery processes that occur during sleep. Most currently prescribed hypnotics, such as the benzodiazepines and Z-drugs, suppress SWA. Some compounds have been shown to enhance SWS and SWA in healthy volunteers through GAT-1 inhibition, GABA-A modulation, GABA-B modulation, and 5HT2(A) antagonism. Pharmacological enhancement of SWS has also been observed in insomnia. The effects of SWS enhancement on other sleep parameters will be discussed.