ABSTRACTThe purpose of this study was to test the hypothesis that latency of REM onset is a negative function of drug‐induced precentral fast (18 to 26 cps) activity in the EEG. Chlorpromazine increased this activity during sleep and wakefulness and decreased latency of REM sleep, whereas α‐chloralose, pentothal, and phenobarbital were associated with a decrease of this activity during sleep, increased slow wave sleep, and increased latency of REM sleep. Phenobarbital and pentothal increased this fast activity during wakefulness and drowsiness, respectively. However, 18 to 26 cps precentral activity was reduced during sleep with α‐chloralose and pentothal. A supporting study in cats demonstrates apparent synchrony of fast activity in the limbic system and cortex during wakefulness, and chlorpromazine increases fast activity in the limbic system. It is speculated that chlorpromazine enhances the effect of the limbic system on cortical (primarily precentral) activity. The sedatives are thought to potentiate the spontaneous slow wave sleep