Sleep disturbance is a common complaint in alcoholics. When polysomnographi
c studies are performed in alcoholics, reductions in slow wave sleep are a
common finding; however, few studies have evaluated the effects of chronic
alcohol exposure on sleep in animal models. In the present study, the sleep
EEG was evaluated in 40 Wistar rats who were exposed to chronic alcohol or
control conditions in vapor chambers. Rats were exposed to ethanol vapors
or control chambers for 6 weeks and then withdrawn. Sleep EEG was recorded
before exposure (baseline), immediately following exposure, and 5 weeks aft
er withdrawal from the ethanol/control chambers. In the ethanol-exposed ani
mals, blood ethanol levels averaged 192 mg/dL over 6 weeks of exposure. Chr
onic ethanol exposure and withdrawal was not found to affect either slow wa
ve sleep latency or slow wave sleep duration; however, overall spectral pow
er as well as power in the delta, theta, and beta frequencies were signific
antly reduced following chronic exposure (2-4 Hz, [F(1, 17) = 18.11, p = 0.
001], 4-6 Hz, [F(1, 17) = 15.98, p = 0.001], 6-8 Hz [F(1, 17) = 15.52, p =
0.001], 8-16 Hz band [F(1, 17) = 18.73, p < 0.0001], 16-32 Hz [F(1, 17) = 1
0.13, p = 0.005], and 1-50 Hz [F(1, 17) = 17.03, p = 0.001]. After 5 weeks
of withdrawal, significant decreases still persisted in the delta and theta
frequencies (2-4 Hz [F(1, 16) = 6.21, 0.024], 4-6 Hz [F(1, 16) = 6.26, 0.0
24]. and 6-8 Hz [F(1: 16) = 4.84, p = 0.043]). These findings suggest that
spectral analysis of the EEG is a highly sensitive measure of the effects o
f ethanol on sleep. These findings additionally demonstrate that chronic et
hanol exposure can produce persistent diminution in the systems that genera
te cortical slow waves in the rat and thus may provide a model for understa
nding the mechanisms underlying sleep disturbances associated with alcoholi
sm. (C) 2000 Elsevier Science Inc. All rights reserved.