Enhancing Slow Wave Sleep 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