The purpose of this study is to determine if there the impact of sleep deprivation upon sleepiness, attention, memory, and mood is reduced by pharmacologically enhancing slow wave sleep (SWS) with sodium oxybate.

SWS has been hypothesized to be a time of relatively high neural recuperation from wakefulness. That hypothesis has been prompted by a number of observations, including: 1) enhanced SWS following sleep deprivation in proportion to the duration of prior wakefulness, 2) reduced amounts of SWS during nocturnal sleep following afternoon/evening naps, 3) a gradual decline in SWS across a night of sleep, and 4) increased SWS following nights of fragmented sleep. Within the two-process model of sleep regulation, heightened SWS has been viewed as reflecting Process S, the homeostatic component. Many authors have proposed that increased SWS represents ongoing cortical recovery from prior wakefulness activities and is a time of relatively heightened neurophysiologic restoration or recuperation. In a prior study which we conducted (Walsh et al., 1994) there was a suggestion, from post hoc analyses, that SWS may prevent adverse effects of sleep loss. Additionally, we recently published the results of an investigation of pharmacologically-enhanced SWS (with tiagabine) during sleep restriction which demonstrated preserved neurobehavioral performance despite sleep restriction (Walsh et al, 2006). In the proposed research we will examine whether pharmacological enhancement of SWS with sodium oxybate reduces the impact of sleep deprivation upon sleepiness, attention, performance, mood, and autonomic nervous system activity.

Inclusion Criteria:

1. males and females, ages 18-50 inclusive
2. use of adequate contraceptive procedures throughout the study for females.

Exclusion Criteria:

1. pregnancy or lactating
2. prior use of or allergy to sodium oxybate
3. participation in a clinical research trial within the past 30 days
4. blood donation within the past 30 days